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CRRAB 1 Week 3 > Vascular Control > Flashcards

Vascular Control Flashcards

1
Q

How do shorter-term and long-term control regulating vascular smooth muscle differ?

A

short-term involves vascular adjustments made by regulating contractile activity of vascular smooth muscle cells.

Long-term adaptatoin includes remodeling of smooth muscle and connective tissue in the vascular wall

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2
Q

Smooth muscle cells arein all vascular tissue except what?

A

capillaries

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3
Q

Why is vascular smooth muscle unique among smooth muscle?

A

it must sustain active tension for prolonged periods:

  1. contract and relax slowly
  2. can change contractile activity based on action potentisl or RMP
  3. Can chance contractil activity in absence of changes in membrane potential
  4. Can maintain tension for prolonged periods at low energy cost
  5. can be activated by stretch
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4
Q

How are smooth muscle cells arranged in the blood vessel wall?

A

circumferentially - some connected with gap junctions

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5
Q

How do the muscle fibers of vascular SM cells differ from other muscle types?

A
  1. not arranged in regular, repeating sarcomere units
  2. actin filaments are longer and connect at inner surface of cell
  3. where the actin filaments connect are called dense bodies,
  4. No Z lines
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6
Q

What are the steps in the contractile process once Ca2+ is in the cell?

A
  1. Ca2+ complexes with calmodulin
  2. this complex activates myosin light-chain kinase
  3. MLC kinase allows ATP to phosphorylate MLC protein
  4. MLC phosphorylation enables cross-bridge formation and cycling - tension development and shortening
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7
Q

Vascular smooth muscle depends on what then?

A

the net state of myosin light chain phosphorylation

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8
Q

What is the “latch state”

A

slow or non-cycling cross-bdiges which minimize the need for ATP

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9
Q

What is the resting membrane potential of vascular smooth muscle? Determined by what ion permeability?

A

-40 to -65 mV

determined by K+ permeability (predominantly via the K+ rectifier channel, but also ATP=dependent K channels)

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10
Q

APs in vascular smooth muscle are typically a result of inward movement of what ion?

A

Ca2+

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11
Q

Intracellular Ca2+ concentrations can change with or without changes in membrane potential. How do they change WITH the membrane potential?

(electrochemical coupling)

A

they’re voltage-gated Ca2 channels, so membrane depolarization opens them, Ca2+ come sin and you get a contraction

If the RMP is low, you don’t get as many Ca2+ channels open and you alter basal contractile states

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12
Q

Describe the pharmacomechanical coupling of the vascular smooth muscle cells.

A

Chemical agents can induce smooth muscle contraction without changing the membrane potential because they open receptor-mediated Ca2+ channels

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13
Q

What is the mechanism for VSM relaxation with electromechanical route?

A

hyperpolarizaiton of the membrane

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14
Q

What is the mechanism for VSM relaxation with the pharmacomechanica route?

A

the chemical vasodilators that target a G-PCR with second messenger effects leads to increased cAMP and cGMP. this ultimately will stimulate Ca2+ EFFLUX, so you get a negative feedback loop

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15
Q

What is the basal tone or intrinsic tone?

A

the state of partial constriction that the arteriole remains in even after removal of all external influences

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16
Q

What is the theory behind why and how basal tone occurs?

A

occurs because the vessels want to actively resist stretch from the continual internal pressure

tonic production of local vasoconstrictor substances by endothelial calls

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17
Q

What is the most important means of local flow ocntrol?

A

metabolic - arteriols and their VSM are subject to the chemical composition of the organ they serve

18
Q

What are some chemical signals to stimulate vasodilation?

A 
low O2
High CO2
High H+
High K+
Release of adenosine
19
Q

What local hormone is produced by endothelial cells to cause vasodilation?

A

nitric oxyde (produced via NO synthase form L-artginine in response by a rise in Ca2+ concentrations)

20
Q

What does NO do?

A

it easily diffuses across the cell membrane and stimulates cGMP production.

21
Q

What are some other substances that can stimulate NO production?

A

acetylcholine, bradykinin, vasoactive intestinal peptide

22
Q

Arterioles are actively and passively responding to changes in transmural pressure - slight passive distansion causes what? How about a suden increase in transmural pressure?

A

slight - activates constriction that reverses the distention

sudden - the opposite

23
Q

What is active hyperemia?

A

when you have increased blood flow because the organ it’s going to really needsit due to a highly variable metabolic rate. (skeletal and cardiac)

24
Q

What is reactive hyperemia?

A

higher than normal blood flow after removal of a restriction

25
Q

What is autoregulation?

A

nearly all organs tend to keep their blood flow constant despite variations in arterial pressure

if arterial pressure increases, they will constrict their arterioles so that resistance increases and the flow remains constant

26
Q

What provides the most important means of RELFEX control fo vasculature?

A

sympathetic vasoconstrictor nerves

27
Q

What receptor does NE bind to in the sympathetic innervation on vascular smooth muscle to cause constriction? Dilation?

A

alpha-1 adrenergic for constriction
Beta-2 for dilation

(note the beta-2 are more sensitive, so moderate epi levels lead to vasodilation and high levels lead to vasoconstriciton)

28
Q

When is vasopressin released into the blood from the posterior pituitary gland?

A

in response to low blood volume and/or high extracellular fluid osmolarity

29
Q

What does vasopressing (ADH) do>

A

it acts on the ducts in the kidneys to decrease renal excretion of water

also acts as a potent arteriolar vasoconstrictor

30
Q

Wat does angiotensin II do?

A

is regulates aldosteron release form the adrenal cortex as part of a Na+ balance control mechanism

acts a sa potent vasoconstrictor (but shouldn’t be viewed as a normal regulator of arterial tne)

31
Q

How is control of venous tone inherently different from control of arterial tone?

A

it’s not subject to local metabolic needs

32
Q

Which volume - central venous or peripheral venous has the most influence on SV and CO?

A

central blood volume (but peripheral affects central, so it’s all connected)

33
Q

There is very little basal tone in venous tissue, so how does blood pump through?

A

the walls are thin and susceptible to physical influences, so muscles pump the blood back to the heart during exercise

34
Q

In what organs is vascular control totally controlled by metabolic mechanisms?

A

brain, heart, skeletal muse

35
Q

In what organs is vascular tone totally controlled by sympathetic vasoconstrictor nerves?

A

kidneys, skin and splanchnic organs

36
Q

What is the most important driving force for coronary blood flow? What is the most important influence on coronary blood flow?

A

driving force = systemic arterial pressur

influeence = myocardial O2 consumption

37
Q

Wht happens to coronary arterioles when symptahtetic neural activity increases?

A

they dilate! even though they are innervaed with sympathetic vasoconstricto fibers!

this is because the increased sympathetic tone increases mocardial O2 consumptoin by increases HR and contractility and the metabolic influences trump the SNS in terms of coronary blood flow!

38
Q

What are the characteristics of vascular sontrol in skeletal muscle blood flow?

A
  1. there’s a high level of intrinsic vascular tone
  2. there is a resting state
  3. there is an exercising state where local metabolic ocntrol is the most important
39
Q

General increase in sympathetic activity leads to what in skele muscle vasculature?

A

increase in sympathetic activity limtis the degree of metabolic vasodilation to prevent excessive reduction in the total peripheral resistance. so they dilate to an extent, but the symptathetic keeps them constricted to an extent

40
Q

In cerebral blood flow, what is the primary trigger for vasoconstriciton?

A

decreased partial pressure of CO2

you’ll get vasodilation in decreased partial pressure of O2

41
Q

SPlanchnic blood flow is largely controlled by sympatheti cneural activity. Maximal SNS activation can produce how much of a reduction in flow to this region?

A

80%! reduction!

it shifts the blood back tot he central venous system

CRRAB 1 Week 3 (7 decks)

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