Heller Ch. 7 Flashcards

1
Q

How does contraction/relaxation of smooth muscle compare to that of striated muscle?

A

Smooth muscle is slower

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2
Q

Besides rate of contraction, what other differences are there between smooth and striated muscles?

A

Smooth can change contractile activity and can maintain tension for prolonged periods of time (Latch state)

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3
Q

What is step 1 of cross-bridge cycling in smooth muscle?

A

Calcium and calmodulin form complex

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4
Q

What happens after the calcium/calmodulin complex is formed in cross-bridge cycling of smooth muscle?

A

The complex activates myosin light-chain kinase

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5
Q

What does the myosin light-chain kinase do in cross-bridge cycling of smooth muscle?

A

Phosphorylates the light chain (at head of myosin) via an ATP

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6
Q

What does the phosphorylated myosin head do for cross-bridge cycling of smooth muscle?

A

Uses energy from ATP to develop tension and shorten

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7
Q

Which two potassium channels are used in determining the RMP of smooth muscle cells?

A

Inward rectifying-type

ATP dependent–open if ATP levels fall

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8
Q

What kind of calcium channel is used in depolarization of smooth muscle cels?

A

Voltage-operated (VOC)

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9
Q

What two potassium channels are used in REpolarization of smooth muscle cells?

A

Delayed

Calcium-activated

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10
Q

What type of channel is used in electromechanical coupling?

A

VOCs

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11
Q

What type of channel is used in pharmacomechanical coupling?

A

Receptor-Operated Channels (ROCs)

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12
Q

How does electrochemical coupling lead to contraction?

A

Membrane depolarization–>increased open-state of channels–>contraction

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13
Q

What causes changes in calcium influx rate? What does changing the influx rate cause?

A

Changes in RMP cause changes in calcium influx rate

Changes in calcium influx rate changes the basal contractile state

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14
Q

What is basal tone?

A

Constant state of partial constriction

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15
Q

How does ACh effect the vascular system?

A

If endothelium is intact, it dilates

If endothelium is stripped, it constricts

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16
Q

How does ACh stimulate vasodilation?

A

Increases concentration of NO–>increased GMP production–>vasodilation (process is unknown)

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17
Q

What other vaso-effectors are affiliated with endothelial cells?

A

Prostacyclin (vasodilator)

Endothelin (vasoconstrictor)

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18
Q

What is the local metabolic vasodilator hypothesis?

A

Tissue cells secrete vasodilator factors to increase flood flow proportional to how much they need

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19
Q

How does prostaglandin effect vascular tone?

A

Can be a dilator (inflammation) or constrictor (from platelets)…just depending

20
Q

What does histamine do to vasculature?

A

Vasodilator via cAMP pathway

Increases vascular permeability (causes edema)

21
Q

Which is a better vasodilator, histamine or bradykinin?

A

Bradykinin by 10 fold

22
Q

What is the active response to hyperemia?

A

Increased blood flow (exercise) causes slight dilation to reduce pressure followed by a quick constriction back to normal

23
Q

What is the reactive response to hyperemia?

A

Blood flow is reduced (tourniquet), then the obstruction is removed and the artery over-compensates blood flow and then constricts back to normal size

24
Q

What is autoregulation of blood flow?

A

Keep blood flow constant

25
Q

What is the metabolic theory of autoregulation?

A

A “washout” of vasodilators from the interstitium by the excess initial blood flow

26
Q

What is the myogenic theory of autoregulation?

A

Increase in arteriole tone stimulated by the increase in stretching forces

27
Q

That is the tissue pressure theory of autoregulation?

A

Increased arterial pressure–>increased transcapillary fluid filtration–>increased interstitial fluid volume and pressure–>compression of vessels

28
Q

What is neurogenic tone?

A

Tonic activity of sympathetic vasoconstrictor increases contractile tone

29
Q

What does epinephrine binding to β2-adrenergic receptor cause?

A

Vasodilation (opposite of most catecholamine actions)

30
Q

What does norepinephrine binding to β2-adrenergic receptor cause?

A

Nothing…β2-adrenergic receptors are not innervated

31
Q

What does vasopressin do?

A

Decreases renal excretion of water

Potent arteriolar constrictor

32
Q

What does angiotensin II do?

A

Regulates aldosterone release from the adrenal cortex…regulates blood volume
Very potent vasoconstrictor

33
Q

Do vasodilators have much of an effect on veins?

A

No…veins lack basal tone

34
Q

Which organs primarily regulate blood flow by metabolic control?

A

Brain
Cardiac muscle
Skeletal muscle

35
Q

Which organs primarily regulate blood flow by neurogenic control?

A

Kidneys
Skin
Splanchnic organs

36
Q

When can sympathetic control effect skeletal muscle blood flow?

A

Both during rest and during exercise–to prevent BP from dropping too much (prevent fainting)

37
Q

How much oxygen does resting muscle need?

A

Not much

Flow can be greatly reduced without damaging tissue

38
Q

What has a greater effect on venous return, contracting muscles or sympathetic activity?

A

Contracting muscles

39
Q

How much does brain blood flow change throughout a day?

A

Hardly at all…pretty constant

40
Q

How much of an effect does sympathetic stimulation have on renal blood flow?

A

A huge amount…flow can be reduced to basically nothing

41
Q

What is pulmonary arterial pressure relative to the rest of the arteries in the body?

A

Significantly lower (1/7)

42
Q

How can the pulmonary arterial pressure be so low?

A

There is very little resistance…there can be the same amount of flow with a lower pressure

43
Q

What do pulmonary arterioles do during hypoxia?

A

Constrict (systemic arterioles would dilate)

44
Q

What possibly causes the pulmonary response to hypoxia?

A

Prostaglandin synthesis

45
Q

What is the effect of vasoconstriction during pulmonary hypoxia?

A

Greater vascular resistance and pulmonary arterial hypertension

46
Q

What is the role of autonomic nerves in the pulmonary system?

A

Very little