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Undeleted > Lecture 21: Local Control of Blood Flow (Hayward) > Flashcards

Lecture 21: Local Control of Blood Flow (Hayward) Flashcards

1
Q

greatest resistance to flow is in

A

arterial circulation

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2
Q

fx of gap junctions in blood vessels

A

transfer excitation to adjacent cells

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3
Q

What is vessel tone derived from?

A

Sympathetic, hormonal, and intrinsic mechanisms

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4
Q

Smooth muscle contractility compared to striated m.

A

contracts and relaxes more slowly

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5
Q

smooth muscle tension compared to striated m.

A

can maintain tension for prolonged periods w/low energy cost

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6
Q

myogenic response

A

activates smooth muscle contraction in response to stretch

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7
Q

Normal RMP for smooth muscle

A

between -50 and -70mV

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8
Q

Changes in K+ –> smooth muscle

A

can cause local changes in constriction. However, primary AP is produced by Ca

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9
Q

Myosin light chain kinase (MLCK)

A

phosphorylates myosin light chains (MLC) in presence of ATP. This will enable the myosin crossbridge to bind to the actin filament and allow contraction to begin. Since smooth muscle does not contain a troponin complex, as striated muscle does, this mechanism is the main pathway for regulating smooth muscle contraction.

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10
Q

How is MLCK inactivated?

A

decreasing intracellular Ca+ (muscle contraction does not stop however because MLC has already been physically modified)

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11
Q

How does smooth muscle that was contracted via MLCK mech. relax?

A

Dephosphorylation of the myosin light chain (and subsequent termination of muscle contraction) occurs through activity of a second enzyme known as MLCP (Myosin Light Chain Phosphatase).

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12
Q

MLC phosphorylation leads to:

A

cross-bridge formation and muscle contraction (actin and myosin interact)

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13
Q

What molecule is NOT involved in vascular smooth muscle contraction that IS involved in striated muscle contraction?

A

troponin

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14
Q

vascular smooth muscle relaxation

A

1) Decreased intracellular Ca
2) MLCK dephosphorylation
3) increased cGMP, which inhibits Ca influx
4) Beta-2 receptor binding and increases in cAMP triggers Ca++ transfer to extracellular space/inhibits MLCK phosphorylation

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15
Q

What do beta-2 receptors bind and then cause?

A

Primarily epinephrine. Cause vasodilation, increase in cAMP

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16
Q

increases in cGMP and cAMP cause

A

vasodilation

17
Q

What does norepinephrine primarily bind to?

A

alpha receptors

18
Q

What does epinephrine primarily bind to?

A

beta receptors (some alpha too)

19
Q

stretched vessel –> Ca channels

A

open Ca channels, causing local vessel constriction

20
Q

4 types of intrinsic mechanisms in vessels

A

1) metabolic regulation
2) myogenic mech.
3) mechanical compression
4) endothelial dependent regulation

21
Q

What does mechanical compression of vessel (intrinsic mech.) cause?

A

restriction on metabolites being flushed to/from vessel

22
Q

What does endothelial dependent regulation do?

A

locally releases gas to act on smooth muscle layer

23
Q

myogenic mechanism

A

How arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow within the blood vessel constant.

The smooth muscle of the blood vessels reacts to the stretching of the muscle by opening Ca channels, which cause the muscle to depolarize, leading to muscle contraction.

24
Q

hyperemia

A

increase of blood flow to different tissues in the body

25
Q

More O2 in circulation results in

A

vasodilation

26
Q

Less O2 in circulation results in

A

vasoconstriction

27
Q

where/when does most mechanical compression occur?

A

coronary vessels during systole and during strong skeletal muscle contractions

28
Q

gradually increasing duration of arterial occlusion on limb —-> flow when cuff is released

A

greater flow when cuff is released. More time occluded = more flow to correct it when cuff is released

29
Q

what is endothelial system sensitive to?

A

shear stress and pressure. Causes vasodilation and decreased velocity

30
Q

most potent vasoconstrictor **

A

endothelin

31
Q

relationship between endothelial layer and smooth muscle layer has a great effect on

A

vasodilation

32
Q

what gas is released from endothelium to smooth muscle layer to vasodilate?

A

NO

33
Q

endothelin

A

most potent vasoconstrictor. Produced by endothelial cells. Released in response to changes in pressure in the system

34
Q

What does endothelin bind to?

A

ETa and ETb receptors

35
Q

What happens when endothelin binds to ETa receptors?

A

vasoconstriction, inotropic/chronotropic effects mediated

36
Q

What happens when endothelin binds to ETb receptors?

A

vasodilation

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