Lecture 8 Flashcards

1
Q

How does the sympathetic system increase relaxation rate?

A

Phospholambam phosphorylation and troponin I phosphorylation

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2
Q

How does sympathetic system increase the rate of muscle contraction?

A

Phosphorylated VOCC.

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3
Q

What are T tubules?

A

Invaginations of muscle cell membranes.

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4
Q

Describe how the architecture of muscle cells increases efficiency?

A

VOCCS are located within T tubules and the SR is close by. The RyR on the SR is close to the VOCCs so trigger calcium activates CICR quickly.

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5
Q

What are class V anti-arrhythmic drugs?

A

Cardiac glycosides.

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6
Q

What do cardiac glycosides do?

A

They inhibit the Na+/K+ pump. This stops removing sodium so the intracellular sodium concentration rises and the cell depolarises. to reverse this the Na/Ca exchanger reverses to remove Na and brings calcium into the cell. This acts as trigger calcium at the RyR. Cardiac glycosides are positive inotropes. E.g. digoxin which is used for congestive heart failure.

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7
Q

What is an example of a class IV drug?

A

Verapamil. It is a calcium channel blocker. Negative inotrope. They treat hypertension and angina.

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8
Q

What is the main intrinsic muscle regulation?

A

The Frank-starling mechanism

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9
Q

Describe starlings law

A

Increased filling pressure leads to an increased end-diastolic volume. This increases stroke volume (force of contraction has to increase). Cardiac muscle cells stretch more which makes them more sensitive to calcium and increase force.

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10
Q

How does increased stretch achieve increased force of contraction?

A

More overlap of actin and myosin filaments therefore greater number of cross-bridges formed. At optimal length for contraction, actin filaments no longer overlap each other and can interact with myosin. This does not occur in skeletal muscle because at resting level, the sarcomers are already at optimal length.

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11
Q

Change in pre-load

A

Lie down suddenly, more blood enters right atrium. EDV and atrial filling pressure has increased.

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12
Q
A
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