Cardiac & Smooth Muscle Flashcards

(27 cards)

1
Q

Neurogenic vs Myogenic?

A

Contraction caused by action potential from motor neurons or an intrinsic electrical rhythm in the muscle itself.

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2
Q

Describe the myogenic rhythm of the SA node

A

SA node cells’ membrane potential fluctuates from -60mV immediately following an action potential, then slowly falls to about -50mV - threshold potential. Time to peak of the ensuing action potential is about 50ms, and the whole things lasts about 150-200ms.

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3
Q

What is pacemaker potential?

A

Describes the slow depolarisation following that precedes the cardiac action potential. It’s gradient plays a major role in determining heart rate, and is modulated with nerves & hormones.

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4
Q

What is the effect of vagus nerve stimulation.

A

This hyperpolarises the membrane of the SA node cells, briefly inhibiting/delaying the next cardiac action potential and slowing heart rate.

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5
Q

What is the effect of cardiac sympathetic nerves stimulation?

A

This increases the gradient of the slope of the pacemaker potential, quickening heartrate.

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6
Q

What causes the pacemaker potential?

A

When membrane potential becomes greater than -50mV, this causes a specific type of Na+ channel to open, causing a slower flow of Na+ that opposes the flow of K+ ions causing repolarisation of the SA node cells. Resulting slow depolarisation triggers a Ca2+ current that sums with Na+ to accelerate depolarisation until action potential is triggered.

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7
Q

What causes the SA node action potential?

A

unlike atrial or ventricular myocytes, the action potential is the result of increase membrane permeability to Ca2+ rather than Na+. Influx of these ions causes a potential reversal. Repolarisation results from increasing K+ and falling Ca2+ permeability until hyperpolarisation and pacemaker potential repeating.

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8
Q

Why can’t cardiac muscle be tetanised?

A

Due to the long duration of the cardiac action potential, the mechanical response of the muscle occurs while the muscle membrane remains depolarised. As one action potential must end before another can begin, this prevents summation - allows time for filling.

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9
Q

Describe the role of Ca2+-induced Ca2+ release in myocytes

A

During the plateau phase of the cardiac action potential, the influx of Ca2+ ions through voltage gated channels on the plasma membrane of the myocytes stimulates them to release their SR stores of calcium. Unlike skeletal, cardiac muscle in a solution lacking calcium won’t contract.

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10
Q

Relationship between contraction force and stretch in cardiac muscle

A

Even closer relationship than in skeletal muscle. Force increases as cardiac muscle is stretched to up to 40% longer than resting length. Stretch is usually determined by venous return, but also sometimes blood pressure, so that normally the heart pumps all the blood it receives.

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11
Q

Define chronotropic regulation

A

Changes in heart rate mediated by sympathetic SAN innervation and circulating epinephrine.

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12
Q

Define inotropic regulation

A

Changes in contractility (force of contraction) mediated by sympathetic SAN innervation and circulating epinephrine. Intrinsic contractility (inotropic state) of the heart determines its efficiency as a pump.

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13
Q

Describe the positive inotropic effect on cardiac muscle.

A

No similar effect in skeletal muscle, occurs with no change in muscle length. Adrenergic receptors binding adrenaline results in Ca2+ influx into cardiac muscle, resulting in cAMP generation, activating protein kinase A, phosphorylating the Ca2+ channels of the plasma membrane and keeping them open for longer.

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14
Q

How do action potential shapes differ around the heart?

A

In the SA node, amplitude of action potential small, 70-80 mv, and the diastolic membrane potential has a
characteristic wave form (pacemaker potential). In the myocardium of the atria and ventricles, the action potential is large, 100-110 mV, and diastolic membrane potential steady (at about -90 mV). 


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15
Q

Structure of cardiac muscle

A

Cardiomyocytes are striated, branched and multicellular. At intercalated disks the cells are connected together mechanically by desmosomes (fascia adherens) and electrically by gap junctions - functional syncytium.

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16
Q

What do mitochondria of cardiac muscle indicate?

A

The higher numbers of mitochondria in cardiac vs skeletal muscle indicates the importance of aerobic metabolism, preventing fatigue - as does the high capillary density between cells.

17
Q

Smooth muscle structure

A

Sheets of spindle shaped uninucleated cells joined by dense bands for mechanical and gap junctions for electrical coupling. Actin and myosin filaments run obliquely across the cells arranged in a loose lattice. Thin and intermediate filaments attach to dense bodies which replace Z-lines. Caveolae make up for no T-tubules and less SR.

18
Q

Role of cytoskeletal intermediate filaments in smooth muscle

A

assist in transmission of force generated during contraction to neighbouring cells and connective tissue.

19
Q

Differences in innervation of smooth and skeletal muscle

A

Smooth muscle innervated by autonomic not somatic. Autonomic nerve fibre varicosities replace motor nerve endings and are sometimes bundled within the bulk of the muscle rather than associated with a few cells. neurotransmitter is released into interstitium not a specific synaptic region, as receptors are distributed all over the cells.

20
Q

Describe and give examples of single-unit smooth muscle

A

cells are grouped loosely into 3D clusters, and due to gap junctions behave as a functional syncytium. Smooth muscle of the gut, uterus and bladder.

21
Q

Define myogenic contractures

A

In some smooth muscle tissues, such as the gut, spontaneous contractions originate in specific pacemaker areas.

22
Q

Describe hormone-smooth muscle interactions during pregnancy

A

During pregnancy, myometrium activity is reduced by circulating progesterone, decreases expression of proteins (e.g. connexin 43) involved in gap junction formation. Estriol does the exact opposite and is important during parturition.

23
Q

Quirks of excitation contraction coupling in smooth muscle

A

Na+/K+ permeability ratio is 1:5 as opposed to 1:100 in skeletal, so resting membrane potential is more like -50mV. Depolarisation results from a varying blend of Ca2+ and Na+ influx. Action potential 5-10 times longer (50ms) and sometimes has a prolonged plateau like in cardiac.

24
Q

Describe role of pacemaker cells in smooth muscle

A

These show spontaneous fluctuations of potential called slow waves. During an excitatory phase, slow wave activity builds until potential falls below about -35mV threshold where series of action potentials is generated.

25
How smooth muscle pacemaker cell activity modulated?
(Para)sympathetic nerves often regulate activity. In the intestine, PARAsympathetic ACh causes depolarisation that means slow waves are more likely to exceed threshold - increasing activity. Sympathetic has an inhibitory effect through hyperpolarisation. Elsewhere these effects reverse. Pacemaker activity is unaffected.
26
How does Ca2+ stimulate contraction of smooth muscle?
Activation of contraction by calcium is not via troponin as in skeletal muscle, but through an enzyme, myosin light chain kinase in conjunction with calmodulin (calcium binding protein). This enzyme phosphorylates sites on myosin cross-bridges, so inducing interaction of cross-bridges with actin, and contraction; relaxation occurs after removal of calcium and is due to dephosphorylation of myosin by a phosphatase.
27
What is stress relaxation or plasticity of smooth muscle?
When stretched, smooth muscle tension increases immediately, then slowly decreases back towards initial value. When tension is decreased (e.g. emptying bladder), it initially falls then returns to original level thus maintaining tone in the walls of hollow organs of greatly changing volume - smooth muscle able to shorten by 2/3 original length as opposed to skeletal's 1/5.