CV and ANS

Question 1

Thin filaments in myocytes are made of (3 things):

Answer 1

Actin, tropomyosin, troponin

Question 2

Thick filaments are made of:

Answer 2

myosin heavy and light chains

Question 3

The interaction of thick and thin filaments in the contraction of heart cells is called the _______ theory.

Answer 3

sliding filament

Question 4

When Ca++ binds to troponin, what happens to tropomyosin?

Answer 4

It moves off of the actin chain, exposing a site for cross-bridging with the myosin head

Question 5

Is the heart electrically excited by neurons?

Answer 5

No

Question 6

Ach binds to […] receptors in motor end plate for skeletal muscle to initiate the muscle action potential

Answer 6

Ach binds to nicotinic cholinergic receptors in motor end plate for skeletal muscle to initiate the muscle action potential

Question 7

There is a flux of [ion name] ions through Ach receptors to initiate the skeletal muscle action potential.

Answer 7

There is a flux of Na+ ions through Ach receptors to initiate the skeletal muscle action potential.

Question 8

If you do not have Ca++ surrounding a heart cell will it continue to beat?

Answer 8

No (classic result by Sydney Ringer in 1883 w/ frog heart)

Question 9

Does skeletal muscle contraction require a Ca++ influx?

Answer 9

No. In skeletal muscle all the Ca++ for contraction is released from the sarcoplasmic reticulum.

Question 10

What happens to skeletal muscle during a series of action potentials at high frequency?

Answer 10

Tetanus (sustained contraction)

Question 11

Label the lines and bands in this diagram

Question 12

In smooth muscle are actin and myosin structured into sarcomeres?

Answer 12

No, therefore it appears histologically “smooth”

Question 13

Does smooth muscle contain troponin? What must happen to the myosin light chain so that it can interact with actin in smooth muscle?

Answer 13

No; the myosin light chain must be phosphorylated to interact with actin in smooth muscle

Question 14

In smooth muscle, can you have a contraction without an action potential?

Answer 14

Yes

Question 15

Which two boundaries does the Ca++ in smooth muscle cross to create a contraction event?

Answer 15

• membrane Ca++ channels (voltage-gated and not)
• Ca++ is released from sarcoplasmic reticulum

Question 16

What enzyme phosphorylates the myosin light chain in smooth muscle cells? What is it activated by?

Answer 16

Myosin light chain kinase (MLCK); activated by Ca++ bound to calmodulin

Question 17

Does β-adrenergic stimulation relax or contract smooth muscle, in general?

Answer 17

Relax

Question 18

Does nitric oxide contract or relax smooth muscle, in general? What is a drug that participates in this functionality?

Answer 18

Relax; Viagra

Question 19

Does α-adrenergic stimulation usually contract or relax smooth muscle?

Answer 19

Contract

Question 20

In which zone of the sequence of cardiac electrical activation does the impulse travel slowest?

Answer 20

The AV node (creates the delay between atrial and ventricular contraction)

Question 21

Are the Purkinje fibers more similar to the ventricles or the atria in terms of the shape and timing of the action potential during a contraction cycle?

Answer 21

The ventricles; the atria correspond more closely with the SA and AV node.

Question 22

What is happening during stage 3 of this action potential in the ventricles?

Answer 22

Repolarization.

Question 23

Would this be a ventricular or an SA node myocyte? How can you tell?

Answer 23

SA node; it’s skinny and there are no striated fibers. Compare with ventricular:

Question 24

Do healthy ventricular cells fire spontaneously?

Answer 24

No, they will stay at the resting potential of -85mV indefinitely.

Question 25

Is this an SA node or ventricular action potential? What’s the easiest way to know?

Answer 25

SA node; the depolarization phase would be much faster in ventricle

Question 26

In this experiment, electrical stimuli are delivered at the points shown in part a. What is the name of the period between the dash-dotted lines in part b?

Answer 26

The RRP or Relative Refractory Period; a strong stimulus can trigger a weak action potential in this period.

Question 27

What is the name of the period during which it is impossible to trigger a second action potential in a cardiac myocyte?

Answer 27

Absolute Refractory Period. This is the reason the heart cannot go into tetanus (prolonged contraction) the way skeletal muscle can.

Question 28

Which ion moves into the cell during the rapid depolarization of a ventricular action potential? Immediately afterward? How about during the plateau and repolarization?

Answer 28

Na+ in during depolarization, Ca++ in right afterward, K+ out during repolarization

Question 29

What ion is influxing during phase 0 of this SA nodal action potential?

Answer 29

Ca++

Question 30

What is the E_K for a cardiomyocyte?

Answer 30

Approx -89mV.

Question 31

If V across the membrane is greater than E_X, does the positive ion X move into or out of the cell?

Answer 31

Positive current; ion moves out.

Question 32

Based on this experiment measuring Na+ current at different test potentials across the membrane of a cardiomyocyte, at what membrane potential do Na+ channels begin to open?

Answer 32

-60mV

Question 33

Which E_X is the cardiomyocyte closest to at resting potential?

Answer 33

E_K (around -85mV)

Question 34

As Na channels open at -60mV, and current begins to flow, does the current increase or decrease the voltage across the membrane?

Answer 34

Increase, thus driving more Na current, and creating a positive feedback system

Question 35

What is the current (which ions) described by the black and top red curves here?

Answer 35

I_Na and I_Ca

Question 36

After the transient [direction] K+ current in an action potential in the cardiomyocyte, there are delayed rectifier currents [direction].

Answer 36

After the transient outward K+ current in an action potential in the cardiomyocyte, there are delayed rectifier currents inward.

Question 37

If you block delayed rectifier currents for K⁺ with a drug, what would happen to the action potential?

Answer 37

It is prolonged

Question 38

[loss or gain of function] mutations in K+ channels or [loss or gain of function] mutations in Na+, Ca2+ channels can cause “Long QT” syndrome.

Answer 38

Loss-of-function mutations in K+ channels or gain-of-function mutations in Na+, Ca2+ channels can cause “Long QT” syndrome.

Question 39

During the plateau of the action potential, which ion current mirrors Ca⁺⁺?

Answer 39

K⁺ in the opposite direction (outward)

Question 40

[ion] links electrical activation to mechanical contraction in heart cells.

Answer 40

Calcium links electrical activation to mechanical contraction in heart cells.

Question 41

During each heartbeat, calcium both enters the cell through […] and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

Answer 41

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

Question 42

During each heartbeat, calcium both enters the cell through membrane channels and is released from the […]. Most of the calcium is released from the latter.

Answer 42

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

Question 43

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the [former or the latter].

Answer 43

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

Question 44

[cellular structure] in heart cells allow for calcium to rise uniformly throughout large myocytes.

Answer 44

Transverse tubules in heart cells allow for calcium to rise uniformly throughout large myocytes.

Question 45

In the resting state for a cardiomyocyte, is more Ca⁺⁺ in the extracellular space, within the cytosol, or in the sarcoplasmic reticulum?

Answer 45

Extracellular space.

Question 46

Is contraction of the heart cell during, before, or after the Ca⁺⁺ influx? Is the action potential during, before or after the Ca⁺⁺ influx?

Answer 46

Contraction is after, action potential is before.

Question 47

What is the structure pointed to by the huge black arrow in this diagram of a cardiomyocyte?

Answer 47

transverse tubule (T-tubule)

Question 48

What is the spacing between T-tubules in a cardiomyocyte?

Answer 48

2μm

Question 49

What is the purpose of having T-tubules spaced every 2μm in the ventricular myocyte?

Answer 49

It places all locations in the ventricular myocyte within 1μm of the cell membrane so that Ca⁺⁺ can reach them quickly

Question 50

Do Purkinje fibers need to contract in order to ensure proper heart function?

Answer 50

No, they main function is electrical propagation. But they do contract somewhat.

Question 51

The following shows changes in Ca⁺⁺ concentration along the longitudinal axis of two different kinds of cardiomyocytes, over the time course of a contraction cycle. Based on this picture, what can you say about T-tubules in Purkinje cells?

Answer 51

Purkinje cells usually don’t have T-tubules, so Ca⁺⁺ must diffuse in from the periphery.

Question 52

Ca⁺⁺ can be pumped out of the cardiomyocyte using active transport channels that transfer the ions in one direction, but how else can it enter and leave the cell?

Answer 52

Sodium-calcium exchangers (NCXs), which symport 3 Na⁺ ions in one direction in exchange for one Ca⁺⁺. These can act much quicker than other modes of transport.

Question 53

Do sodium-calcium exchanges (NCXs) change the membrane potential? Do they require ATP?

Answer 53

Yes, there is a net transfer of +1 charge into the cell. They do not require ATP, but the Na⁺ gradient is usually created by a different ATP-consuming symporter, the Na⁺/K⁺ ATPase.

Question 54

T-tubules may alter their shape from state E to state F, shown below. Would this change enhance or detract from heart function?

Answer 54

Detract; it is more difficult to initiate Ca⁺⁺ release from the sarcoplasmic reticulum if the T-tubules are unevenly spaced

Question 55

What does inotropy mean? What is an inotrope?

Answer 55

Intropy: contractility, the force of muscle contraction. Inotrope: an agent that changes this. Greek: Inos, fiber. Trope, turning.

Question 56

The following is the treatment strategy for Digitalis, intended to increase inotropy. What is the problem with this strategy?

Answer 56

Cardiotoxicity, because: not only are you knocking out Na⁺/K⁺ ATPases somewhat nonspecifically, but increased intracellular Ca⁺⁺ can cause spontaneous Ca⁺⁺ release from the sarcoplasmic reticulum, which produces uncontrolled cardiac contractions.

Question 57

What does SERCA (sarco-endoplasmic reticulum Ca⁺⁺-ATPase) do? What happens if it is inhibited?

Answer 57

It transfers Ca⁺⁺ from the cytosol to the lumen of the sarcoplasmic reticulum (SR) during muscle relaxation, in preparation for its release from the SR during muscle contraction. Inhibition of SERCA impairs muscle contraction.

Question 58

[sympathetic or parasympathetic] stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Answer 58

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Question 59

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in [cell type in heart] cells.

Answer 59

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Question 60

[sympathetic or parasympathetic] stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Answer 60

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Question 61

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in [cell type in heart] cells.

Answer 61

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

Question 62

What does chronotropy mean?

Answer 62

Heart rate (Greek: chronos, time. Tropo, turning.)

Question 63

Sympathetic stimulation […] ventricular contractility ([…] inotropy) due to phosphorylation of multiple targets and increased intracellular calcium

Answer 63

Sympathetic stimulation increases ventricular contractility (positive inotropy) due to phosphorylation of multiple targets and increased intracellular calcium

Question 64

Increased heart rate leads to […] ventricular contractions ([…] inotropy) through […] intracellular calcium

Answer 64

Increased heart rate leads to stronger ventricular contractions (positive inotropy) through increased intracellular calcium

Question 65

Heart failure leads to [shorter or longer] action potentials, weaker contractions, and an altered response to sympathetic stimulation

Answer 65

Heart failure leads to longer action potentials, weaker contractions, and an altered response to sympathetic stimulation

Question 66

Heart failure leads to longer action potentials, weaker contractions, and an altered response to [sympathetic or parasympathetic] stimulation

Answer 66

Heart failure leads to longer action potentials, weaker contractions, and an altered response to sympathetic stimulation

Question 67

What does dromotropy mean?

Answer 67

Cell-to-cell conduction; Greek: dromos, running. Tropos, turning.

Question 68

Are the cardiac effects of parasympathetic inhibition greater OR less than the effects of sympathetic inhibition? What does this tell you about the tone of cardiac muscle?

Answer 68

Parasympathetic is greater. This means cardiac muscle has parasympathetic tone.

Question 69

A heart transplant patient has decreased “default” innervation of the heart–therefore, what would the change in heart rate be compared with typical patients?

Answer 69

It would be faster, due to less basal vagal stimulation.

Question 70

Which has faster effects, parasympathetic or sympathetic stimulation of the heart?

Answer 70

Parasympathetic is faster

Question 71

Are parasympathetic effects on the heart due to nicotinic, muscarinic, or adrenergic receptors?

Answer 71

Muscarinic receptors (M₂ to be specific)

Question 72

Parasympathetic stimulation affects the SA node via 1) [activation or inhibition] of acetylcholine-sensitive K current, 2) inhibition of funny current I_f, and 3) decreased sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Answer 72

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current I_f, and 3) decreased sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Question 73

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) [activation or inhibition] of funny current I_f, and 3) decreased sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Answer 73

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current I_f, and 3) decreased sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Question 74

What parts of the heart express the funny current?

Answer 74

Mostly the spontaneously active regions, like the SA node, AV node, and Purkinje fibers.

Question 75

Does increasing cAMP levels increase or decrease the open probability of f-channels, the channels that convey the funny current?

Answer 75

Increase

Question 76

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current I_f, and 3) [increased or decreased] sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Answer 76

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current I_f, and 3) decreased sarcoplasmic Ca⁺⁺ release by inhibiting SERCA.

Question 77

What region of the heart is mediated by sympathetic effects but not parasympathetic effects?

Answer 77

The ventricles

Question 78

Where are ryanodine receptors located? What do they do?

Answer 78

Sarcoplasmic reticulum membrane; they control release of intracellular Ca⁺⁺ stores.

Question 79

Are ryanodine receptors more likely or less likely to release Ca⁺⁺ in the sarcoplasmic reticulum if the concentration of Ca⁺⁺ on the cytosolic side is higher? Is this a positive or negative feedback system?

Answer 79

More likely to release Ca⁺⁺ with higher cytosolic levels; this is positive feedback

Question 80

What controls the open or closed state of an L-type calcium channel? Where are they located and why are they important to muscle cells?

Answer 80

They are voltage gated, so at a certain membrane potential they open. They are located in the cellular membrane. In muscle cells, they control Ca⁺⁺ influx from the extracellular space.

Question 81

What kind of receptor are L-type calcium channels coupled to in striated muscle and what membrane are those receptors embedded in?

Answer 81

The L-type calcium channel in the cytoplasmic membrane is coupled to a ryanodine receptor (RyR) in the sarcoplasmic reticulum, facilitating simultaneous flow of Ca⁺⁺ from both compartments into the cytoplasm

Question 82

Do ECG electrodes detect intracellular or extracellular voltages?

Answer 82

Extracellular

Question 83

Which histological structure stains strongly for connexin 43 protein in cardiomyocytes, the main constituent of cardiac gap junctions?

Answer 83

Intercalated disks

Question 84

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage […]. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

Answer 84

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

Question 85

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only [location] potential over a distance.

Answer 85

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

Question 86

A signal minus a time shifted version of itself is a rough [mathematical function] of the signal. This is why the ECG signal is roughly proportional to the [mathematical function] of the the action potential.

Answer 86

A signal minus a time shifted version of itself is a rough derivative of the signal. This is why the ECG signal is roughly proportional to the derivative of the the action potential.

Question 87

Depolarization moving towards a positive electrode gives an [up or down] deflection.

Answer 87

Depolarization moving towards a positive electrode gives an upward/positive deflection.

Question 88

What kind of deflection does an orthogonal waveform produce as measured by two electrodes?

Answer 88

No deflection/signal.

Question 89

The T-wave appears as a positive deflection because the endocardium is activated [before or after], but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant V_endo-V_epi looks like a T wave.

Answer 89

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant V_endo-V_epi looks like a T wave.

Note how the black line is above the red during the repolarization (tail end) of the action potentials, and that subtracting red from black would result in an upward bump. That is the T-wave.

Question 90

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes [before or after] the epicardium. When the differences in signal and time are taken into account, the resultant V_endo-V_epi looks like a T wave.

Answer 90

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant V_endo-V_epi looks like a T wave.

Note how the black line is above the red during the repolarization (tail end) of the action potentials, and that subtracting red from black would result in an upward bump. That is the T-wave.

Question 91

Why do you not see a signal for atrial repolarization on an ECG? (The T wave is the signal for ventricular repolarization).

Answer 91

Atrial repolarization is too slow with respect to time, and the atrial mass is too small; the signal is not significant enough to be visualized on the ECG

Question 92

The strength of a given signal depends not only on propagation direction, but also on the [physical property] of tissue contributing to the signal

Answer 92

The strength of a given signal depends not only on propagation direction, but also on the mass of tissue contributing to the signal

Question 93

Which part of the PQRST wave on an ECG corresponds with atrial depolarization?

Answer 93

The P wave

Question 94

Why aren’t there any ECG signals from conducting tissues, e.g. the AV node or Purkinje fibers?

Answer 94

Not enough mass.

Question 95

As the ventricles depolarize, what is the motion of the vector representing the averaged direction of propagation of the action potential through the tissue?

Answer 95

A counterclockwise circle

Question 96

When reading a paper ECG, how many large boxes indicate a second?

Answer 96

5.

Question 97

What’s going on in this ECG? Hint, look at the red lines.

Answer 97

The P-R interval is too long (240 ms, should be <200ms), this indicates first degree AV block. First degree means delayed, not blocked.

Question 98

What’s wrong with this ECG?

Answer 98

There’s a P wave without a QRS! This is 2nd degree AV block

Question 99

What is this waveform called?

Answer 99

Atrial fibrillations: P waves are random and indistinct, R-R intervals are irregular

Question 100

What are the large weird waveforms in this ECG? (Assume nobody is bumping the leads) How many ectopic foci are there?

Answer 100

These are premature ventricular contractions, or PVCs. There are multiple ectopic foci since the PVCs have different shapes.

Question 101

What is this heart rhythm called?

Answer 101

Monomorphic ventricular tachycardia. Monomorphic because all complexes are similar

Question 102

What does ventricular tachycardia reflect?

Answer 102

Either ventricular focus, or reentry

Question 103

What is cardiovascular reentry mean?

Answer 103

When signals are propagated from a Purkinje twig to muscle, if they propagate much faster through one branch than another, they can start circling back through other branches and re-stimulate ventricular tissue

Question 104

What is this heart rhythm called? Without intervention, how long does the patient have to live?

Answer 104

Ventricular fibrillation; patient could die in minutes

Question 105

How do you convert mMol/L to mEq/L?

Answer 105

Multiply it by the valence of the ion and then by the relative number of the ion from the empirical formula.

Question 106

How do you convert from mMol/L to mOsm/L?

Answer 106

Multiple by the number of ions in the molecule

Question 107

What’s the typical total body fluid volume? How much is intracellular? How about extracellular?

Answer 107

40L total, intracellular 25L, extracellular 15L

Question 108

What’s the typical blood volume, and how much of it is plasma?

Answer 108

5L blood, 3L plasma

Question 109

What’s the primary ion in extracellular fluid? How about intracellular fluid?

Answer 109

Na⁺ extracellular, K⁺ intracellular

Question 110

What does the Morse equation calculate?

π = gCRT

Answer 110

Osmotic pressure

Question 111

When using Morse’s equation, typically a correction factor σ is added to correct for a small permeability of capillaries to certain proteins. What is the range of this correction factor?

π = σgCRT

Answer 111

0 to 1, depending on the capillary boundary in question

Question 112

Does water move toward high osmotic pressure or away from it?

Answer 112

Toward it, as it is defined as the amount of (hydrostatic) pressure needed to keep the fluid out in this experimental setup:

Question 113

Are GI secretions hypertonic, hypotonic, or isotonic?

Answer 113

Isotonic except for saliva which is hypotonic

Question 114

Is sweating hypertonic, hypotonic, or isotonic

Answer 114

Hypotonic. It tastes salty because it evaporates quickly.

Question 115

What are Starling’s forces?

Answer 115

1. Hydrostatic pressure.
2. Oncotic (osmotic) pressure.

Question 116

What is the primary neurotransmitter of the parasympathetic system?

Answer 116

Acetylcholine

Question 117

What is the primary neurotransmitter at neuromuscular junctions, excluding muscles with sympathetic tone? What are the receptor types for smooth vs. skeletal muscle?

Answer 117

Acetylcholine; nicotinic receptors at skeletal, muscarinic at smooth

Question 118

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is […].

Answer 118

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

Question 119

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter […] which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

Answer 119

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

Question 120

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates […] receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

Answer 120

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

Question 121

Does parasympathetic stimulation cause bronchoconstriction or bronchodilation? Via what receptor?

Answer 121

Bronchoconstriction, via M₃ (muscarinic) receptors

Question 122

Sympathetic innervation uses noradrenaline as the primary neurotransmitter at the end organ or gland with two exceptions. What are they?

Answer 122

1) Sweat glands: acetylcholine –> muscarinic receptor
2) Renal vascular smooth muscle: dopamine –> dopamine receptor

Question 123

What is the primary neurotransmitter and receptor at ganglia for both the sympathetic and parasympathetic nervous system?

Answer 123

Acetylcholine, nicotinic receptor

Question 124

Blood flow through the circulatory system is driven by gradients in blood pressure. Blood vessels exhibit both […] and compliance.

Answer 124

Blood flow through the circulatory system is driven by gradients in blood pressure. Blood vessels exhibit both resistance and compliance.

Question 125

Connecting blood vessels in [series or parallel] decreases the overall system resistance; conversely,
connecting blood vessels in [series or parallel] increases the overall system resistance.

Answer 125

Connecting blood vessels in parallel decreases the overall system resistance; conversely,
connecting blood vessels in series increases the overall system resistance.

Question 126

The resistance of a blood vessel is determined primarily by its [physical property].

Answer 126

The resistance of a blood vessel is determined primarily by its radius.

Question 127

Is the vascular pressure in the aorta higher or lower than in the vena cava?

Answer 127

Higher

Question 128

Water flow can be related to current (from electromagnetism). What is the pressure difference analogous to?

Answer 128

Voltage. Q = ΔP/R ⇔ I = V/R

Question 129

Velocity is [relationship operator] to flow and inversely proportional to cross-sectional area of the vessel.

Answer 129

Velocity is proportional to flow and inversely proportional to cross-sectional area of the vessel.

Question 130

Velocity is proportional to flow and [relationship operator] to cross-sectional area of the vessel.

Answer 130

Velocity is proportional to flow and inversely proportional to cross-sectional area of the vessel.

Question 131

Blood vessel resistance is inversely proportional to the [N]th power of vessel radius.

Answer 131

Blood vessel resistance is inversely proportional to the 4th power of vessel radius.

Question 132

Does increased hematocrit increase, decrease, or not change blood viscosity?

Answer 132

Increase

Question 133

When vessels are more “stretchy”, are they more compliant or less compliant? Given constant volume, is what is the relationship between compliance and pressure?

Answer 133

More compliant. Inversely. C = V/P.

Question 134

Are arteries more compliant or less compliant than veins? How can compliance be estimated from the following curves?

Answer 134

Arteries are less compliant; Compliance is equivalent to the slope of these curves

Question 135

Capillaries are very small, so they are extremely high resistance (resistance is inversely proportional to the 4th power of radius). Why isn’t the capillary bed the area of greatest resistance in the circulatory system?

Answer 135

The ~3 billion capillaries are in parallel, which knocks out their overall contribution of resistance to the system

Question 136

Which section of the vasculature presents the greatest resistance? How do we know this?

Answer 136

Arterioles: we know this because there is the greatest pressure drop across this segment

Question 137

Is the greater resistance of arterioles due to their smooth muscle?

Answer 137

No, it is purely the geometry of connectivity; the smooth muscle does mean that the resistance can be regulated by arterioles, redirecting flow.

Question 138

Cardiac valves open and close in response to changes in [physiological variable] in cardiac chambers and blood vessels

Answer 138

Cardiac valves open and close in response to changes in blood pressure in cardiac chambers and blood vessels

Question 139

From tracings of pressure and volume versus time, loops of pressure versus volume can be created. Changes in [physiological variable] can be understood from changes in pressure-volume loops.

Answer 139

From tracings of pressure and volume versus time, loops of pressure versus volume can be created. Changes in cardiac output can be understood from changes in pressure-volume loops.

Question 140

The [name] relationship describes the fact that increased filling of the ventricle will increase cardiac output.

Answer 140

The Frank-Starling relationship describes the fact that increased filling of the ventricle will increase cardiac output.

Question 141

Increased filling pressure (preload) leads to [increased or decreased] cardiac output.

Answer 141

Increased filling pressure (preload) leads to increased cardiac output.

Question 142

Increased pressure in arteries (afterload) leads to [increased or decreased] cardiac output.

Answer 142

Increased pressure in arteries (afterload) leads to decreased cardiac output.

Question 143

Increased afterload will decrease the degree of muscle shortening.

Increased preload will [increase or decrease] the degree of muscle shortening.

Answer 143

Increased afterload will decrease the degree of muscle shortening.

Increased preload will increase the degree of muscle shortening.

Question 144

What is the name of this kind of diagram?

Answer 144

The classic “wiggers” diagram

Question 145

In this wiggers diagram, what does the top red line correspond to? What is happening during the “bump”? Which valve is opening and closing on either side of it?

Answer 145

The aortic pressure; ejection is occuring during the bump, and the aortic valve opens and closes on either side of it.

Question 146

Why would the mitral valve close at this point of the Wiggers diagram? Keep in mind the blue line is the left ventricular pressure and the pink is left atrial pressure.

Answer 146

The left atrial pressure drops below the left ventricular pressure, so there can be no forward flow through the valve; retrograde flow closes the mitral valve.

Question 147

When the mitral valve opens at this point, what starts happening to ventricular volume?

Answer 147

It rises, this is when the heart fills.

Question 148

At each corner of this curve, what is the valve that is opening or closing?

Question 149

What is the stroke volume represented in this diagram? How about the systolic blood pressure?

Answer 149

~65 mL and 115 mmHg

Question 150

Why is the diastolic blood pressure at this corner of the PV loop?

Answer 150

This is when the aortic valve opens during systole; in other words, when ventricular pressure has just exceeded aortic pressure. Aortic (and blood) pressure is at a minimum just before ejection begins and therefore, this pressure is the diastolic blood pressure.

Question 151

The end-diastolic pressure volume relationship is measure by tracking which corner of the PV curve?

Answer 151

The bottom right.

Question 152

The end diastolic pressure and volume are in which corner of the PV loop?

Answer 152

The bottom right corner.

Question 153

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the […] relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

Answer 153

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

Question 154

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a [greater or smaller] slope.

Answer 154

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

Question 155

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume [increases or decreases] and thus cardiac output [increases or decreases] with increased preload.

Answer 155

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

This indicates a weaker heart or risk of heart failure.

Question 156

If the end-systolic pressure volume relationship has a [high or low] slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

Answer 156

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

This indicates a weaker heart or risk of heart failure.

Question 157

What physiological perturbations alter preload?

Answer 157

Increased venous return, which is affected by venous tone and the volume of circulating blood.

Question 158

Should the slope of the end-systolic pressure volume relationship change under typical physiological variations throughout the day, e.g. ingestion of a meal or physical activity? If not, what does affect the slope?

Answer 158

No. It’s a reflection of the limits of the contractility of heart tissue, which (generally) does not respond to changes in preload or afterload. This is why it is a reliable diagnostic indicator. Inotropic drugs can affect contractility, however.

Question 159

Under normal physiological conditions, which vasculature system affects afterload?

Answer 159

Arterial system

Question 160

Does increased peripheral vascular resistance increase or decrease afterload?

Answer 160

Increase

Question 161

What sort of pharmacological agents or endogenous regulators would affect afterload?

Answer 161

Vasoconstrictors and vasodilators: agents that affect peripheral vascular resistance.

Question 162

If contractility of a heart increases given the same preload and afterload, what happens to cardiac output?

Answer 162

It increases (dramatically)

Question 163

What physiological perturbations can affect contractility?

Answer 163

1) Sympathetic stimulation of the ventricles
2) Increased circulating Ca⁺⁺
3) Myocardial hypertrophy (growth of heart muscle)

Question 164

Why is ejection fraction used to measure contractility in heart patients instead of the end systolic pressure volume relationship (ESPVR)?

Answer 164

To get the ESPVR you need to measure left ventricular pressure and volume accurately while subjecting the heart to different loads. Measuring ventricular pressure is fairly invasive so it is usually only done in animal studies.

Question 165

How do you calculate ejection fraction from a pressure volume loop? How is it related to the slope of the end systolic pressure volume relationship (ESPVR)?

Answer 165

Ejection fraction = stroke volume / end diastolic volume. It roughly correlates with ESPVR slope, but as you can see in the following curve it will be a very rough correlation.

Question 166

Is preload or afterload a greater confounding variable for the clinical use of ejection fraction to measure contractility of heart muscle?

Answer 166

Afterload is a worse confounder. As can be seen in the following curves, increasing afterload can decrease the ejection fraction. (remember, EF = SV/EDV) Increasing the preload can change ejection fraction, but generally not as much (it depends on the EDPVR curve).

Question 167

When […] receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Answer 167

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Question 168

When nicotinic receptors on the adrenal medulla are activated by […], epinephrine and norepinephrine are released into the blood.

Answer 168

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Question 169

When nicotinic receptors on the [organ part] are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Answer 169

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Question 170

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, [hormone] and [hormone] are released into the blood.

Answer 170

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

Question 171

Cholinergic transmission occurs in three primary sites; what are they?

Answer 171

1) Pre-ganglionic fibers in the sympathetic and parasympathetic systems
2) Post-ganglionic fibers in the parasympathetic system
3) Somatic nerves at the neuromuscular junction

Question 172

What is taken up via a sodium-dependent transporter in order to be synthesized into acetylcholine via a reaction with acetyl coenzyme-A (AcCoA) and what enzyme performs this reaction?

Answer 172

Choline; the enzyme is choline acetyltransferase

Question 173

Acetylcholine is stored in synaptic vesicles by what transporter?

Answer 173

Vesicle Associated Transporter (VAT)

Question 174

In the synapse, what enzyme breaks down acetylcholine? What happens when this enzyme is inhibited?

Answer 174

Acetylcholinesterase; inhibitors would prolong the action of acetylcholine.

Question 175

Why would there be acetylcholine receptors on the presynaptic terminal of a cholinergic synapse?

Answer 175

Regulation of neurotransmitter release

Question 176

What two classes of membrane proteins coordinate synaptic vesicles to the synaptic membrane for release?

Answer 176

SNAPs and VAMPs

Question 177

What amino acid is the precursor for dopamine, norepinephrine, and epinephrine synthesis?

Answer 177

Tyrosine

Question 178

What transporter stores noradrenaline, adrenaline, and domaine into vesicles within presynaptic terminals?

Answer 178

Vesicular Monoamine Transporter (VMAT)

Question 179

What transporter facilitates reuptake of catecholamines into the presynaptic terminal?

Answer 179

Norepinephrine transporter (NET)

Question 180

What is the class of molecules that adrenergic receptors respond to?

Answer 180

Catecholamines, which look like catechol + a chain that terminates in an amine. This is catechol:

Question 181

What is the primary function of α1 adrenergic receptors? What is their primary location in the periphery?

Answer 181

Smooth muscle contraction; blood vessels of the skin and GI tract, so the result is vasoconstriction in these areas

Question 182

What are the primary functions of β1 adrenergic receptors in the heart?

Answer 182

Increases heart rate, cardiac contractility and conduction

Question 183

What does activation of β₂ adrenergic receptors do in blood vessels?

Answer 183

Small muscle relaxation; Vasodilitation

Question 184

Does acetylcholine have a higher affinity for muscarinic receptors or nicotinic receptors?

Answer 184

Muscarinic

Question 185

If blood pressure increases, baroreceptors sense this, and [increase or decrease] their firing to [increase or decrease] parasympathetic and [increase or decrease] sympathetic input to the heart. This [increases or decreases] heart rate.

Answer 185

If blood pressure increases, baroreceptors sense this, and increase their firing to increase parasympathetic and decrease sympathetic input to the heart. This decreases heart rate.

Question 186

What is the primary tone of blood vessels?

Answer 186

Sympathetic

Question 187

What is the primary adrenergic receptor type in bronchiolar smooth muscle and the blood vessels of skeletal muscle?

Answer 187

adrenergic β₂

Question 188

What is the primary receptor for parasympathetic signals to the heart?

Answer 188

Muscarinic, M₂

Question 189

Does sympathetic activity open or close the iris? Which muscle does it use? Which receptor?

Answer 189

Open; iris radial muscle; adrenergic α1 receptor

Question 190

What is the action of parasympathetic stimulation of the iris (dilation or constriction)? Which muscle(s) does it contract? Which receptor is involved?

Answer 190

Constriction; iris circular muscle and ciliary muscle; muscarinic M3 receptor

Question 191

Why are postsynaptic receptors often ligand-gated channels?

Answer 191

Upon binding of the ligand (the neurotransmitter) ions rush through the channel, starting a postsynaptic action potential

Question 192

If acetylcholine receptors line the edges of junctional folds within a neuromuscular junction, what lines the depths of the folds and why?

Answer 192

Acetylcholinesterase, to break down the neurotransmitter and terminate stimulation of the muscle

Question 193

What receptor family do the β-adrenergic receptors belong to? Via which enzyme do they act to increase intracellular cAMP?

Answer 193

G-protein coupled receptors; adenylyl cyclase

Question 194

Which part or layer of the adrenal gland releases epinephrine?

Answer 194

The medulla

Question 195

When epinephrine binds to β₂ adrenergic receptors, what happens? Which tissues carry this receptor?

Answer 195

The smooth muscle in bronchioles and a subset of blood vessels (mostly to skeletal muscle) relax.

Question 196

For which adrenergic receptor does norepinephrine significantly lack agonist activity? How does this make its effects different from those of epinephrine?

Answer 196

β₂ adrenergic receptors; therefore, it does not cause dilation of blood vessels in some skeletal muscles

Question 197

What are the targets of isoproterenol? Is it an antagonist or an agonist?

Answer 197

Adrenergic β-receptors (both β1 and β2). It is an agonist.

Question 198

Which receptors are targeted by phenylephrine? What are its physiological effects?

Answer 198

Adrenergic α1 and α2 receptors. It causes vasoconstriction in many blood vessels, and lowers heart rate.

Question 199

What are the series of events leading to phenylephrine’s effect of lowered heart rate?

Answer 199

Phenylephrine causes vasoconstriction, which causes baroreceptors to detect an increase in SBP. They fire more frequently, leading to increased (vagal) parasympathetic and decreased sympathetic stimulation of the heart, decreasing heart rate.

Question 200

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex [heart response].

Answer 200

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

Question 201

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a [increase or decrease] in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

Answer 201

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

Question 202

Phentolamine is a reversible, nonspecific [drug target and agonism]. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

Answer 202

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

Question 203

Beta blockers can be selective or non-selective.

• Metoprolol is a [selective or non-selective] beta blocker that targets [type(s)] receptors.
• Propanolol is a [selective or non-selective] beta blocker that targets [type(s)] receptors.

Answer 203

Beta blockers can be selective or non-selective.

• Metoprolol is a selective beta blocker that targets β1 receptors.
• Propanolol is a non-selective beta blocker that targets β1 and β2 receptors.

Question 204

In the steady state, venous return must [be greater than, equal, be less than] cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

Answer 204

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

Question 205

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve [geometric relationship].

Answer 205

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

Question 206

The venous return curve can be constructed by considering the following: (a) arterial […], (b) arterial compliance, (c) venous compliance

Answer 206

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

Question 207

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial […], (c) venous compliance

Answer 207

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

Question 208

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) […] compliance

Answer 208

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

Question 209

Why does the venous return curve in a Frank-Starling relationship fall with increasing venous/atrial pressure?

Answer 209

Increased atrial pressure makes it harder for venous blood to return to the heart

Question 210

What are the two curves in a Frank-Starling relationship chart?

Answer 210

One is cardiac function, or cardiac output (volume) vs. right atrial pressure; the other is vascular function, or venous return (volume) vs. right atrial pressure

Question 211

What would a decrease in blood volume do to the Frank Starling relationship—what is the predicted effect on right atrial pressure and cardiac output?

Answer 211

Both would fall.

Question 212

What are the two major classes of direct-acting cholinoreceptor stimulants?

Answer 212

Alkaloids and choline esters

Question 213

Where are M₁ receptors principally located? How about M₂ receptors? M₃ receptors?

Answer 213

M₁: nerves;

M₂: Heart, nerves and smooth muscle;

M₃: Glands, smooth muscle and endothelium

Question 214

Which muscarinic receptor acts through activation of K⁺ channels instead of a IP₃/diacyl glycerol cascade?

Answer 214

M₂

Question 215

Nicotinic receptors can be sorted into N_M and N_N type receptors, which are located in skeletal muscle neuromuscular junctions and […], respectively.

Answer 215

Nicotinic receptors can be sorted into N_M and N_N type receptors, which are located in skeletal muscle neuromuscular junctions and post-ganglionic cell bodies, respectively.

Question 216

Nicotinic receptors can be sorted into N_M and N_N type receptors, which are located in […] and post-ganglionic cell bodies, respectively.

Answer 216

Nicotinic receptors can be sorted into N_M and N_N type receptors, which are located in skeletal muscle neuromuscular junctions and post-ganglionic cell bodies, respectively.

Question 217

Which muscarinic receptor type is targeted by vagus stimulation of the heart?

Answer 217

M₂

Question 218

What physiologic effects on the heart would be expected from a parasympathetic agonist?

Answer 218

Negative chronotropy (lower heart rate), inotropy (decreased contractility in the atria), and dromotropy (decreased conduction velocity).

Question 219

Alkaloids are structurally recognizable by what feature?

Answer 219

Nitrogen containing rings.

Question 220

What are the sites of action of a nicotinic agonist?

Answer 220

1) gangia of both arms of the ANS
2) skeletal muscle neuromuscular junctions

Question 221

What is the structural difference between scopalamine and atropine? What is their targeted receptor(s) and physiological activity?

Answer 221

Scopalamine has an additional oxygen molecule as indicated in this diagram. They are both competitive antagonists for all muscarinic acetylcholine receptors, suppressing parasympathetic stimulation.

Question 222

What is the pharmacological function of atropine? What receptor do they target?

Answer 222

Muscarinic competitive antagonist; they target muscarinic receptors

Question 223

Would atropine cause vasodilation or vasoconstriction? Why or why not?

Answer 223

It causes neither, because although there are muscarinic receptors in blood vessels there are no parasympathetic innervators

Question 224

What is meant by orthostatic hypotension?

Answer 224

A sudden drop in blood pressure when a person stands, by at least 20 mmHg (usually causes some dizziness)

Question 225

What does a ganglionic blocking agent do? What is the classical prototype of these agents?

Answer 225

They blockade both sympathetic and parasympathetic input to organs by acting as a nicotinic antagonist. The classical prototype is hexamethonium, but it is not used clinically because it causes orthostatic hypotension

Question 226

What is the pharmacological mechanism of physostigmine?

Answer 226

It is a carbamylating acetylcholinesterase inhibitor, and it is reversible.

Question 227

How does a neuromuscular blocker like tubocurarine (curare) work at the molecular level?

Answer 227

They are competitive antagonists at skeletal muscle cholinergic nicotinic receptors, preventing opening of the Na⁺/K⁺channels and skeletal muscle contraction.

Question 228

All membrane cotransporters and counter-transporters move ions from [higher or lower] to [higher or lower] electrochemical potential

Answer 228

All membrane cotransporters and counter-transporters move ions from higher to lower electrochemical potential

Question 229

How many ATP does the Na⁺/K⁺ ATPase consumer per cycle? What is the net charge movement (amount and direction)?

Answer 229

One; +1 charge moves out of the cell

Question 230

What are the two transporters that are primarly responsible for maintaining a Ca⁺ gradient between the cytosol and the sarcoplasmic reticulum/extracellular space in a cardiomyocyte?

Answer 230

SERCA (Sarco/Endoplasmic Reticulum Ca⁺⁺ ATPase) and NCX (Na⁺-Ca⁺⁺ exchanger)

Question 231

Is plasma membrane Ca⁺⁺ ATPase (PMCA) important for maintaining the Ca⁺⁺ gradient in cardiomyocytes?

Answer 231

Quantitatively, not really

Question 232

How much of a cardiomyocyte’s ATP is used for myosin movement (contraction)? How about for maintaining ionic homeostasis?

Answer 232

70% for myosin; 30% for maintaining the gradient (via Na⁺/K⁺ ATPase and SERCA)

Question 233

Can the Na⁺-Ca⁺ exchanger (NCX) operate in reverse?

Answer 233

Yes, if the Na⁺ gradient is reversed and there is sufficient Ca⁺ outside the cell, it can reverse direction

Question 234

At equilibrium, the voltage across the membrane will be closest to the Nernst potential of the ion that the membrane is [least or most] permeable to.

Answer 234

At equilibrium, the voltage across the membrane will be closest to the Nernst potential of the ion that the membrane is most permeable to.

Question 235

If contractions of a cardiomyocyte are quickly paced, what happens to the Ca⁺⁺ release over the course of ~20 beats?

Answer 235

It increases

Question 236

What effect would a clinical dosage of norepinephrine have on BP and HR and why?

Answer 236

Increased BP, because of direct effect on α₁ receptors. Norepinephrine has a weak effect on β₁ and barely any effect on β₂ receptors. Usually, the indirect effect of baroreceptor-mediated increased parasympathetic and decreased sympathetic input to heart wins out over the direct β₁ agonism of NE, and HR decreases.

Question 237

What effect does isoproterenol have on HR and BP, and why?

Answer 237

Isoproterenol is a β₁ agonist, increasing heart rate, and a β₂ agonist, vasodilating blood vessels to skeltal muscle and causing a drop in BP.

Question 238

What is the mechanistic difference between β-adrenergic stimulation, as opposed to α-adrenergic stimulation?

Answer 238

β-adrenergic activates adenylyl cyclase, increasing cAMP production; cAMP inhibits MLCK, causing smooth muscle relaxation. α-adrenergic produces IP₃ which increases intracellular Ca⁺⁺, promoting smooth muscle constriction.

Question 239

Of K⁺, Na⁺, and Ca⁺⁺ in the cardiomyocyte, which ion is least affected by digitalis treatment?

Answer 239

K⁺

Question 240

What does phospholamban do? What changes when it is phosphorylated? What phosphorylates it and what upstream branch of the autonomic nervous system controls this?

Answer 240

Phospholamban inhibits the action of SERCA, slowing Ca⁺⁺ uptake into the sarcoplasmic reticulum. When phosphorylated by PKA, this action is inhibited. Increased cAMP and activation of the β₂ adrenergic receptor will activate PKA, phosphorylate phospholamban, and increase Ca⁺⁺ uptake.

Question 241

What is the Nernst equation? What is the approximate value of RT/F in mV? What is z?

Answer 241

RT/F = 25mV

z is the valence of the ion

Question 242

Which ion current does endogenously produced acetylcholine modulate in order to decrease the heart rate?

Answer 242

It increases the amount of repolarizing K+ current that opposes membrane depolarization during phase 4 of the SA nodal action potential.