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CRAAB 3 > Nordgren: Vascular Control > Flashcards

Nordgren: Vascular Control Flashcards

1
Q

Why do we need vascular control?

A

Since the body’s metabolic needs are continually changing the CVS needs to be able to adjust vessel diameter in order to:

  1. Efficiently distribute the CO among tissue w/ different needs (ARTERIAL CONTROL)
  2. Regulate the distribution of blood volume and cardiac filling (VENOUS CONTROL)
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2
Q

How are short term adjustments made in the CVS?

A

Regulating contractile activity of vascular smooth muscle cells

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3
Q

How are long term adjustments made in the CVS?

A

Remodeling of both active (smooth) and passive (structural CT) of the the vascular wall.

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4
Q

Smooth muscle cells are in all vascular tissue EXCEPT…

A

capillaries

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5
Q

Vascular smooth muscle is unique…

A

b/c it must sustain active tension for prolonged periods.

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6
Q

What are the 5 ways that smooth muscle is different from skeletal or cardiac muscle?

A
  1. Contract/relax more slowly
  2. Can change contractile activity based on AP or RMP
  3. Can change contractile activity in absence of any changes in MP
  4. Can maintain tension for prolonged periods at low energy cost
  5. Can be activated by stretch
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7
Q

How are vascular smooth muscle cells arranged?

A
  1. small spindle shaped cells
  2. arranged circumferentially or at small helical angels in muscular walls of a blood vessel
  3. Some are connected to adjacent smooth muscle cells by gap junctions
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8
Q

What is similar about the VSM contractile process to skeletal and cardiac contractile processes?

A

Force and development and shortening is SIMILAR to other muscle types. Cross bridge interactions between thick and thin contractile filaments composed of myosin and actin.

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9
Q

What is different about the VSM contractile process?

A
  1. Not arranged in regular repeating sarcomere units (lacks visible striations)
  2. ACTIN FILAMENTS are much longer
  3. No z lines but DENSE BODIES
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10
Q

What are the sequence of steps that link Ca to contractile filament interaction in VSM?

A
  1. Ca complexes w/ calmodulin
  2. Complex activates myosin light chain kinase
  3. MLC kinase allows ATP to phsophorylate MLC protein
  4. MLC phosphorylation enables cross-bridge formation and cycling–> Energy from ATP is utilized or tension development/shortening
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11
Q

What happens in the latch state of VSM contractile process?

A

Slow or non-cycling cross-bridges minimize the need for ATP

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12
Q

What does VSM contractility depend on ?

A

the NET STATE OF MLC PHOSPHORYLATION

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13
Q

What is the RMP of a VSM membrane and what determines its permeability?

A

-40 - -65

  1. Determined by K permeability
  2. K channel predominantly responsible
  3. Also ATP dependent K channels
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14
Q

APs in VSM are a result of what type of inward current?

A

Ca NOT Na

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15
Q

What does it mean, when it says that VSM can have independent location activation?

A

Activation that occurs in specific vessels that is initiated by slow inward Ca current and are more like pacemakers.

In these cells repolarization occurs by outward flux of K through both the delayed K channels and Ca activated K channels

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16
Q

How does electromechanical coupling occur in VSM?

A

Intracellular free Ca levels can occur WITHOUT changes in membrane potential

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17
Q

How does intracellular free Ca occur without changes in MP? (roles of depol and hyperpol)

A

Voltage operated Ca channels:
Membrane depolarization-> opens VOCs–> Ca in–> Contraction

Hyperpolarization does the opposite

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18
Q

What happens to VOCs at low RMP in VSM?

A

VOCs are partially activated so alterations to RP can alter the basal contractile state.

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19
Q

How do chemical agents induce smooth muscle contraction w/ out the need for change in MP?

A
  1. Receptor operated Ca channels open

2. Formation of inositol triphosphate opens Ca channels on SR

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20
Q

What are the two mechanisms for relaxation?

A
  1. Electromechanical - hyperpolarization of the cell membrane
  2. Pharmacomechanical - Chemical vasodilators target a G protein copuled receptor w/ second messenger effects leading to increased cAMP and cGMP > ultimately stimulate Ca efflux
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21
Q

What do arterioles do?

A

Control the rate of nutritive blood flow through organs and individual regions within them.

INFLOW VALVES

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22
Q

What is vascular tone?

A

Characterizes the general contractile state of a vessel or vascular region (unique feature of VSM)

Used as an indication of the level of activation of the individual smooth msucle cells in that region.

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23
Q

What is Basal tone?

A

ARterioles remain in a state of partial constriction, even after removal of all exernal influences.

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24
Q

What is the mechanism for basal tone?

A
  1. actively resist stretch from continual internal pressure

2. result of tonic production of local vasoconstrictor substances by endothelial cells that line the inner surface

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25
Q

What external influences affect basal tone of CAT?

A
  1. local
  2. neural
  3. hormonal
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26
Q

What are local influences that affect CAT?

A
  1. metabolic
  2. endothelial cells
  3. other chemicals
  4. transmural pressure
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27
Q

How does metabolism locally affect CAT?

A

Arterioles/VSM are subject to the chemical composition of the organ/tissue they serve

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28
Q

What is hte most important means of local flow control on arterioles?

A

Metabolic

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29
Q

What stimulates vasodilation in arterioles?

A

Low 02
High C02, H, K
Release of adenosine

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30
Q

What do endothelial cells locally influence arterioles?

A

They line the entire CV system and produce chemicals that affect tone surrounding smooth muscles.

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31
Q

What do endothelial cells secrete that act on CAT?

A

NO that easily diffuses across cell membrane and stimulates cGMP production.

32
Q

What stimulates NO production?

A

ACh, bradykinin, vasoactive intestinal peptide (their receptors are coupled to ROCa channels)

33
Q

What activates NO synthase?

A

Rise in Ca concentration

L argininge–> NO synthase –> NO

34
Q

What other chemicals locally act on arterioles?

A

PGs and thromboxane
leukotrienes
histamine
bradykinin

35
Q

How does transmural pressure affect the CAT?

A

“Stretch response”

arterioles actively and passively respond to changes in transmural pressure

36
Q

What is a myogenic response?

A

It originates in smooth muscle. D/t activation of stretch sensitive ion channels on arteriolar VSM cells.

occurs when a light passive distension activates constriction taht reverses the distension… a sudden decrease in transmural pressure triggers the opposite response.

37
Q

What is active hyperemia?

A

Blood flow closely follows tissue’s metabolic rate.

  1. Organs w/ highly variable metabolic rate.
38
Q

What does hyperemia mean?

A

FLOW RATE

39
Q

What is reactive hyperemia?

A

Higher than normal blood flow after removal of restriction. The duration depends on severity of occlusion and metabolic needs.

Compensates and tries to deal w/ severity of metabolic needs of tissue that has been restricted.

40
Q

What is autoregulation?

A

Nearly all organs keep their blood floow constant despite variations in arterial pressure. They AUTOREGULATE.

41
Q

How does arterial tone response to a initial increase in a change of pressure that increases Q?

A

A change of Pressure that increases Q causes arterial tone to gradually increase (resistance) and Q to decrease near normal.

42
Q

What are the most important means of reflex control of hte vasculature?

A

Sympathetic vasoconstrictor nerves that innervate arterioles in all systemic organs and are essential in teh global CV regulation of arterial BP.

43
Q

What do sympathetic vasoconstrictor nerves do?

A

Release NE in proportion to AP frequency and can increase tone after combining with α1-adrenergic receptor on smooth muscle cells (pharmacomechanical)

44
Q

What does tonic firing by sympathetic nerves do to arterioles?

A

Increases the normal contractile tone of arterioles to above basal (neurogenic tone)

45
Q

Increased nerve activity =

A

increased vasoconstriction

46
Q

What catecholamines are released into the blood stream by adrenal glands during activation of SNS?

A

Epi and Norepinephrine

47
Q

What do Epinephrine and Norepinephrine do?

A
  1. Activate cardiac β1-adrenergic receptors to increase HR and contractility
  2. Activate vascular α1-receptors to cause vasoconstriction
  3. Vascular β2-adrenergic receptors are more sensitive to epinephrine than are α1-receptors… (Moderate epinephrine levels > vasodilation,
    High epinephrine levels > vasoconstriction)
48
Q

What is vasopressin and where is it released from?

A

ADH released from the pituitary gland

49
Q

Why is vasopressin important?

A

It helps regulate extracellular fluid homeostasis and it’s a POTENT arteriolar VASOCONSTRICTOR.

50
Q

When is vasopressin release?

A

In response to LOW blood volume or HIGH extracellular fluid osmolarity.

51
Q

What does vasopressin act on?

A

Collecting ducts in kidneys to decrease renal excretion of water.

52
Q

What does angiotensin II do?

A

Regulates aldosterone release from the adrenal cortex as part of a Na blanace control mechanism.

53
Q

Why is angiontensin II important?

A

Helps w/ blood VOLUME regulation.

Potent VASOCONSTRICTOR. (Important in CV response to severe blood losss)

54
Q

What may be responsible for abnormal vasoconstriction that accompanies many forms of hypertension?

A

Angiotensin II

55
Q

What is the purpose of venous tone?

A
  1. regulate the distribution of available blood volume between the peripheral and central venous compartments
  2. Has a significant influence on SV and CO–whatever peripheral veins are doing affects the central venous pressure and CO too!
56
Q

Is venous tone subject to local metabolic needs?

A

NO

57
Q

How do VSM in veins differ from arterioles?

A
  1. Very little basal tone–> normally dilated state

2. Thin walls= more susceptible to physical influences

58
Q

What relaxing influences are the SAME in both arterioles and veins of VSM?

A

REFLEX Sympathetic constrictor nerves that release NE that acts on alpha receptors

59
Q

What are the differences in local influences that act on arterioles and veins?

A

Arterioles: thicker
1. Basal tone susceptible to local metabolic influences
2. Vasodilator metaboolites
More tonicity

Veins: thinner

  1. Passively distended state
  2. External compression
60
Q

What tissues are almost totally controlled by metabolic mechanisms?

A

Brain
Heart
Skeletal muscle

61
Q

What tissues are almost totally controlled by sympathetic vasoconstrictor nerves?

A

Kidneys
skin
splanchnic organs

62
Q

What is the driving force for coronary blood flow?

A

Systemic arterial pressure

63
Q

What are the most important factors influencing coronary blood flow?

A

Myocardial O2 consumption

64
Q

What happens to coronary arterioles when sympathetic neural activity increases?

A

They vasodilate

65
Q

How does increased sympathetic tone effect myocardial 02 consumption?

A

It INCREASES IT, by increasing HR and contractility. Metabolic influences always TRUMP SNS.

66
Q

What is the state of vascular tone in skeletal muscle (SO)?

A

High level of intrinsic vascular tone

67
Q

What effects blood flow in skeletal muscle in the resting state?

A

Alterations in SNS activity

68
Q

What effects blood flow in skeletal muscle in the active state?

A

Local metabolic control is the most important!

Generally there is an increase in sympathetic activity–> limits the degree of metabolic vasodilation to prevent excessive reduction in TPR.

69
Q

What leads to unconsciousness and brain damage?

A

Interruption in blood flow for more than a few seconds

70
Q

How is cerebral blood flow regulated?

A

LOCAL mechanisms

  1. Metabolic rate (per gram) is nearly as high as myocardial
  2. blood flow decreases whenever arterial PC02 falls below normal (vasoconstriction) (responds to changes in pH and decreased partial pressure of 02)

*Sympathetic/parasympathetic influences are minimal

71
Q

What is blood flow like to visceral organs?

A

HIGH blood flow, HIGH blood volume (25% of resting CO)

72
Q

What is VERY important for vascular flow through visceral organs?

A

Sympathetic neural activity–maximal acitvation can produce an 80% reduction in flow to this region and shift a large pool of blood back into the venous system

(large fraction of blood shift is d/t venous constriction in the liver)

73
Q

Local metabolic activity is the visceral organs is associated w/…

A

GI motility, secretion, absorption causes vasodilation to increase blood flow to these regions

74
Q

What influences renal blood flow?

A
  1. FLOW important to renal function of regulating the body’s water balance and circulating blood volume
  2. Strongly influenced by SYMPATHETIC neural stimulations
  3. Local METABOLIC MECHANISMS may influence local vascular tone, but mechanisms not clear
75
Q

What regulates cutaneous blood flow?

A
  1. Primary mechanism of flow is the response to METABOLIC STATES and ENVIRONMENTAL CONDITONS that alter TEMPERATURE
  2. One of the largest organs> venous constriction can shift a considerable amount of blood out
  3. Reflex SYMPATHETIC neural activity has important but complex influences on skin blood flow

*SKIN HELPS REGULATE BODY TEMP

76
Q

What regulates pulmonary blood flow?

A

Pulmonary blood flow = CO

  1. Pulmonary arteries constrict in response to LOCAL AVEOLAR HYPOXIA
  2. Autonomic nerves DO NOT play a major role in control of pulmonary vascular activity
77
Q

What is hypoxic vasoconstriction?

A

Diverts blood flow away from underventilated areas so the best ventilated areas receive the most flow.

CRAAB 3 (7 decks)

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