Carduovascular 4 Flashcards Preview

Amars Semester Two cards > Carduovascular 4 > Flashcards

Flashcards in Carduovascular 4 Deck (27)
Loading flashcards...

What role does the Na/K+ ATPase have on the resting membrane?

This is what sets up the concentration gradients for the other ions however it's not involved in the RMP. If you blocked this pump, you would only depolarise the cell by about -7mV


What is the RMP of ventricular myocytes ?

Between -85 and -90mV.


Channels responsible for the ventricular myocyte action potential

Upstroke - opening of V-O-Na channel
Slight downstroke - inactivation of V-O-Na and transient efflux of K+
Plateau - opening of L-type VOCC
Downstroke - closure of VOCC & opening of V-O-K+ channel (K+efflux)


What brings the SAN membrane to threshold?

This is the If - the funny current.
- activated by membrane potentials more negative than -50mV
- the more negative,mother more it activates
- Hyperpolarisation-activated Cyclic Nucleotide-gated channels
- allow influx of Na+ ions


What ion channels are responsible for the upstroke and downstroke of the SAN action potential? (After threshold)

Upstroke is VOCC and downstroke is VO-K+ channels.


Why are VO Na channels not involved in the upstroke of the of the SAN action potential?

The SAN RMP is at roughly -60mV and at this RMP, the VO Na channels would be inactivated - they wouldn't have recovered as the require hyperpolarisation to recover.


What is the RMP of the SAN?



The AVN can conduct AP and the ventricles can also contract on their own. Why does the SAN set the pace of the heart and not the others?

It's quickest to depolarise and so therefore it sets the rhythm and rate of the heart.


Name some key features of cardiac muscle

T-tubules in line with z-lines
Actin and myosin
Centrally located nuclei (max 1 or 2 nuclei per cell)
Intercalated disks.
Gap junctions to allow electrical coupling.
Desmosomes rivet cells together.


What is the predominant source of calcium ions for cardiac myocytes during contraction

NOT the calcium that enters across the Sarcolemma.
The increase in calcium across the Sarcolemma then causes CICR from the sarcoplasmic reticulum
75% from SR
25% from across the Sarcolemma.


How does digoxin work and what effect does it have on the force of comtraction

Increases the force of cotnraction
Inhibits the Na/K ATPase which increases [Na]i
The NCX then reverses and pumps Na+ out and exchanges calcium into the cell.
This increases the amount of calcium available for contraction and so therefore causes a stronger contraction.


Where are the vascular smooth muscles found in blood vessels.

In the tunica media.


In which of the following are vascular smooth muscles not found?



How is myosin light chain kinase activated and what does the activation enable?
Where in the body does this process occur?

- It is activated when calcium is bound to calmodulin ( 4 calcium per calmodulin)
- it phosphorylates MLC which allows myosin to interact with actin.
This process occurs in the regulation of contraction in vascular smooth muscle.


How is MLC inactivated and what does this cause

MLC is dephosphorylated by MLC-phosphatase.
This occurs when calcium levels decline
This will cause relaxation.


What effect does phosphorylation by PKA on MLCK have?

PKA phosphorylation of MLCK inhibits contraction.


What is the effect of stimulation of sweat glands by the parasympathetic nervous system

No effect as its cholinergic by innervated by sympathetic


What receptors does the vagus nerve act on in the heart?

Acts to slow down the heart rate.


What receptor does the sympathetic nervous system innervate in the heart and what's its action?

Innervates B1 adrenoreceptors.
Secretes noradrenaline
+ chronotropic and inotropic effect.


What effects do activation of B1 and M2 receptors have on the SAN? How would each of these appear on the SAN AP graph?

- coupled to Gs - increase PKA and cAMP which activates HCNs
- this increases the HCN flow which brings SAN to threshold quicker
- SAN fires quicker and therefore increases rate of heart
- on the graph, the slope of the HCN will become steep.

- coupled to Gi - which increases K+ conductance and decrease cAMP
- this means it takes longer to bring the SAN to threshold and therefore slows the heart down
- on the graph, the slope to bring to threshold will be shallower and take longer


How does NA have an inotropic effect?

Activation of B1
Increases cAMP and PKA
PKA phosphorylates calcium channels
Therefore increased calcium entry during AP.
More calcium taken into SR so more calcium released for contraction


Why does activation of B2 in the VSM cause vasodilation?

b2 increases PKA
Remember PKA inhibits MLCK
Inhibition means constriction doesn't occur.
Hence vasodilation.


What are stretch receptors, where are they located and how do they relay information regarding blood pressure to the brain?

Nerve endings sensitive to stretch
Located in carotid sinus and aortic arch
Increase pressure stretches them and the information is relayed to brain


There are B2 and A1 receptors in the VSM.
Under which conditions are each receptor active and what is the result

B2 are sensitive to the low concentration of background adrenaline.
Adrenaline has a higher affinity for the B2 so therefore it causes vasodilatation.

At higher concentrations, pharmacological adrenaline has a higher affinity for A1 and so therefore this will cause vasoconstriction.


Name an A1 antagonist and how it's method of action and its effect.

A1 antagonists
Competes with NA for A1 receptor
A1 in VSM, which upon activation cause vasoconstriction
Prazosin blocks NA binding and so causes vasodilation.


Action of propranolol

Non selective beta antagonist
Blocks B1 receptors which normally increase PKA, which phosphorylates HCN channels and VOCC that cause + inotropic and chronotropic effect. Blocking this will reduce the rate and the force.

B2 agonist normally causes PKA increase that activates MLC-phosphatase that dephosphorylates MLC - reducing contraction - hence bronchodilation. When the antagonist is bound, there is less PKA being activated and therefore bronchoconstriction occurs.


What is responsible for the resting membrane potential in cardiac cells?

The open K+ leak channels.
At rest these are open and leak K+ out of the cell therefore bringing the Eq down towards (but not to) the Eq of K+.