Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

► Med - Year 1 > Vascular Smooth Muscle > Flashcards

Vascular Smooth Muscle Flashcards

1
Q

Vascular smooth muscle is found in which vessels, and more importantly, NOT found in which?

A

Arteries, arterioles, veins, and some venules

NOT IN CAPILLARIES!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are pericytes? Where are they found?

A

Contractile cells that wrap around the endothelial cells of capillaries and venules throughout body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What specific part of which vessel contains the greatest relative abundance of vascular smooth muscle?

A

Terminal arterioles (which also have the least elastic tissue of the vessels containing it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are smooth muscle cells arranged around arterioles?

A

Cocentrically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

True or false: Multiple neurotransmitters can be co-released from a nueronal varicosity

A

True (varicosity= swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

(High/Low) density of sympathetic adrenergic varicosities are in arterioles

A

High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which vessels are devoid of sympathetic innervation?

A

Capillaries, postcapillary venules, and small venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are sympathetic adrenergic varicosities close to vascular smooth muscle?

A

Yes, they can be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sympathetic varicosities release multiple neurotransmitters near smooth muscle. List the important 3.

A
  1. Norepinephrine
  2. ATP
  3. Neuropeptide Y
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Net effect of Norepinephrine release

A

alpha1 adrenergic receptor –> PIP2 cascade –> increase [IP3] –> SR Ca release –> vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Net effect of ATP release

A

Purinergic receptor P2x –> ligand gated Ca channel –> Ca influx –> vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Net effect of Nueropeptide Y (NPY) release

A

NPY receptor Y1R –> inhibits adenyl cyclase and activates phospholipase C–> decreases basal PKA –> vasoconstriction

(indirectly allows for more contraction, because PKA isn’t around to phosphorylate and thus inhibit MLCK. MLCK is needed for contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PKA dependent phosphorylation of MLCK (inhibits/activates) MLCK. How?

A

Phosphorylation inhibits MLCK–reduces MLCK’s affinity for Ca-calmodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What occurs wen MLCK is inhibited?

A

no contraction of vascular smooth muscle –> vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In which type of vessel can contraction of a single smooth muscle reduce vessel diameter?

A

Precapillary arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect of contraction of a single smooth muscle cell on mesenteric artery’s diameter?

A

No effect. (mesenteric supplies intestines and pancreas–dont need to supply them/digest when running from mammoth!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The sympathetic nervous system promotes (vasodilation/vasoconstriction) through ___-adrenoceptor mediated elevation of intracellular Ca.

A

alpha1

Note: The source of Ca may vary depending on arterial region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

RyR

A

ryanodine receptor-mediates release of Ca from the SR, essential step in muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Little/many smooth muscles are needed to surround a mesenteric artery

A

many

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

the alpha1-AR signaling pathway for the mesenteric artery involves Ca influx and release form which two sources?

A

RYR and the InsP3R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can inhibit the Ca response in smooth muscles cells surrounding a mesenteric artery?

A

Activation of endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What activates myosin light chain kinase (MLCK)?

A

Calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What inhibits MLCK?

A

cAMP, and phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Does vasoconstriction and vasodilation of vascular smooth muscle require depolarization?

A

NO! It an occur with or without depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

There are multiple mechanisms for modulating intracellular Ca in vascular smooth muscle. List a few

A
  1. Neurotransmitter/hormone –> Gq –> PIP2 –> Ip3 –> Ca release from SR –> Ca/CaM complex
  2. Potential dependent Ca channel
  3. Receptor activated Ca channel by neurotransmitter or hormone
  4. Ca pump, Na/Ca exchanger
26
Q

An agonist may promote vasoconstriction by multiple pathways. We are most familiar with the Gq pathway–what is another important one?

A

Rho and Rho-kinase. Rough idea of cascade:

Agonist –> G12/13 –> GEFs –> Rho-GTP –> Rho-kinase –> phosphorylation of MLC –> contraction

27
Q

PKA promotes (vasoconstriction/vasodilation)

A

Vasodilation (phosphorylates MLCK, decreasing MLCK’s affinity for Ca-Calmodulin)

28
Q

Two ways PKA promotes vasodilation

A
  1. phosphorylation of MLCK

2. activates ATP-dependent K channel, resulting in hyperpolarization

29
Q

Subsarcolemmal calcium sparks–what is their function and mechanism? What can initiate them?

A

They relax smooth muscle by hyperpolarizing the cell by activating a nearby BK(Ca) channel.

Initiated by Arachadonic acid metabolite 11,12 EET.

Note: The sparks are just a little burst of Ca, oterhwise you’d have a contraction.

30
Q

Production of NO by ____ promotes ______

A

endothelial cells, vasodilation

31
Q

eNOS synthesizs NO from L-arginine. What neurotransmitters stimulate this cascade? (4)

A

Acetylcholine, serotonin, thrombin, bradykinin

32
Q

NO release from endothelial cells causes the conversion of what in vascular smooth muscle cell

A

GTP —> cGMP

33
Q

how does cGMP promote vasodilation?

A

activates PKG which promotes:

  1. PKG –> increased myosin phosphatase –> myosin light chain dephosphorylation –> Ca desensitization of actin-myosin interaction
  2. PKG –> increase BK(Ca) –> hyperpolarization –> decrease Ca influx
34
Q

Contraction of vascular smooth muscle is (thick/thin) filament regulated. Why?

A

Thick filament. Requires phosphorylation of a regulatory light chain in myosin by Ca-Cam-MLCK.

Note: THICK filament = myosin. THIN filament = actin. Myosin though has a LIGHT chain.

35
Q

The level of myosin light chain phosphorylation is a balance between which two rates?

A

Rate of phosphorylation by MLCK, and dephosphorylation by myosin phosphatase (MP)

36
Q

Rho kinase pathway can inhibit ____, resulting in wat?

A

myosin phosphatase, resulting in increase of Ca sensitivity of smooth muscle contraction

37
Q

Why is the coronary vasculature pretty resistance to alpha receptors?

A

Don’t want to cose down vasculature of the heart. more beta receptors as a result

38
Q

3 factors allowing smoth muscle relaxation

A

K(ATP) channels, NO, Adenosine

39
Q

Transmural pressure

A

the pressure difference between two sides of a wall

40
Q

When transmural pressure increaes, signaling pathways promote muscle contraction. Why does this occur?

A

Allows arterioles to increase resistance in response to increased blood pressure, to maintain constant blood flow

pressure = flow x resistance

41
Q

What is the purpose of the myogenic reflex?

A

Auto-regulatory mechanism to help maintain flow at a metabolic rate as perfusion pressure increases.

42
Q

Myogenic reflex (does/does not) require the endothelium

A

does not.

43
Q

As transmural pressure increases over time (cm H20), arteriolar diameter (increases/decreases)

A

Decreases (shallow slope)

44
Q

Myogenic reflex involves the following 2 events:

A
  • stretch activated channels

- intracellular signaling

45
Q

In the myogenic reflex, what do stretch channels cause?

A

depolarization, which opens up voltage-gated Ca channels

46
Q

membrane potential of vascular smooth muscle. What does this result in?

A

-40 to -60 mV. Results in basal influx of Ca, hence basal level of contraction

47
Q

Stretch activated channels (2 types)

A
  1. cation channels (TRP, EnaC)

2. chloride channels

48
Q

3 types of intracellular signaling and function

A
  • IP3
  • DAG/PKC
  • RhoA/Rho Kinase

DAG and Rho inhibit MLCP
IP3 causes release of Ca from SR

49
Q

In addition to inhibiting myosin phosphatase, Rho also activates this inhibitor of myosin phosphatase

A

CPI-17

50
Q

Hyperemia is an excess of blood in the vessels. Why does this occur during a baroreceptor vascular reflex?

A

Baroreceptor reflex reacts to decreased pressure (in carotid sinus). A bilateral carotid artery occlusion will increase blood pressure but also will cause a decrease in blood flow.

When the occlusion is released, there is a dramatic increase in flow. The release of the occlusion causes hyperemia–an overshoot–more than you bargained for.

51
Q

What is reactive hyperemia?

A

Increase in blood flow following brief ischemia e.g. arterial occlusion (restriction in blood supply)

52
Q

Why does hyperemia occur? Via what mechanisms?

A

During period of occlusion, tissue hypoxia and vasodilator metabolites build up (i.e. adenosine) –> elevates [cAMP] –> dilate arterioles and decrease vascular resistance. cAMP also activates PKA which inhibits MLCK and causes hyperpolarization via K(ATP).

When occlusion is released, pressure is restored and flow becomes elevated, due to decrease vascular resistance. (pressure = flow x R)

53
Q

When do endothelial cells release nitric oxide?

A

In response to shear stress

54
Q

NO is synthesized in endothelial cells by a

A

Ca-dependent nitric oxide synthetase (L-arginine + O2 –> NO + citrulline)

55
Q

When NO diffuses into smooth muscle cells, what does it activate?

A

Activates guanylate cyclase –> cGMP synthesis –> activates PKG

56
Q

3 ways PKG reduces levels of myosin phosphorylation

A
  1. phosphorylates MLCK (inhibits it)
  2. promoting myosin dephosphorylation
  3. activating BK(Ca) = big K channel, causes hyperpolarization, decrease in Ca influx
57
Q

Thromboxane (TP) promotes (vasodilation/vasoconstriction)

A

vasoconstriction. feeds into PLC and Rho cascades

58
Q

PGI2 (IP) = prostacyclin = prostaglandin = eicosanoid. Function? Mechanism?

A

It inhibits platelet activation and is also an effective vasodilator. Promotes vasodilation by elevating cAMP in vascular smooth muscle –> inhibits MLCK and activates K(ATP)

59
Q

Role of hormone: angiotensin II. What metabolite has same net function?

A

When decreased blood pressure, Angiotensin II will cause an increase in vasoconstriction and help elevate blood pressure.

Thromboxane A2 also promotes vasoconstriction

60
Q

Main determinant of vascular tone

A

Myosin phosphorylation

61
Q

Myosin phosphorylation can by influenced by these 5 mechanisms

A
  1. intracellular Ca –> activates MLCK
  2. inhibition of myosin phosphatase –> increased net myosin phosphorylation
  3. Alter membrane potential: depolarization –> vasoconstriction
  4. increase [cAMP] –> inhibition of MLCK, hyperpolarization (K(ATP)), activation of MP
  5. increase [cGMP] –> activation of MP, hyperpolarization (BKca)
62
Q

three arachidonic acid metabolites and function

A

prostacyclin (PGI2) and 11,12-EET –> vasodilation secondary to hyperpolarization and/or inhibition of MLCK
thromboxane A2 –> vasoconstriction

► Med - Year 1 (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions