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SMP - Cardiopulmonary Exam 1 > Lecture 16 - Neurohumoral Control of Circulation > Flashcards

Lecture 16 - Neurohumoral Control of Circulation Flashcards

1
Q

What are the 2 main NTs of the sympathetic NS? What is each secreted by?

A
  1. Sympathetic nerves release NE at the neuroeffector junction
  2. Adrenal medulla releases EPI
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2
Q

What does the effect of the sympathetic NS on a tissue depend on?

A

Receptors present on the tissue

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3
Q

What are the 3 main adrenergic receptors? What effect does each have?

A
  1. Beta1 = cardiac positive inotropism and chronotropism => increased contractility and HR
  2. Beta2 = vascular dilation
  3. Alpha1 (and alpha2) = vascular contraction
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4
Q

What is the major difference in receptor affinities between NE and EPI?

A

Higher affinity of EPI to beta2 receptors

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5
Q

How do beta1 receptors work?

A

Increase cAMP levels and free intracellular Ca++ levels

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6
Q

How do beta2 receptors work?

A

Increase cAMP levels and decrease of free intracellular Ca++ levels

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7
Q

How do alpha1 receptors work?

A

Increase IP3 levels and free intracellular Ca++

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8
Q

What are the 2 systems in charge of regulating acute moment-to-moment changes in BP?

A

Baro/Chemoreceptors + ANS

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9
Q

What do neurohumoral mechanisms of blood flow control?

A
  1. Regulation of BP and BV over the long-term through regulation of fluid and electrolytes levels
  2. Patterns of flow in regional circulations in a non-uniform manner in altered physiological states: exercise, volume depletion, etc.
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10
Q

Are neurohumoral mechanisms important to short-term BP?

A

NOPE, except under extreme conditions (e.g. hemorrhage)

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11
Q

Describe the regulation of BP via arterial baroreceptor reflex. Purpose?

A

Baroreceptors in the aortic arch and carotid sinus which monitor BP by detecting stretch and then trigger ANS activity adjustment

Purpose: keep arterial pressure constant to provide adequate perfusion to tissues

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12
Q

Describe the steps of the mechanisms of the regulation of BP via arterial baroreceptor reflex.

A
  1. Increase in BP
  2. Baroreceptors in aortic arch/carotid sinus are stretched
  3. Afferent sensory signals sent to medullary cardiovascular center
  4. Reciprocal adjustment of ANS by the medulla to decrease HR = increase in parasympathetic activity and decrease in sympathetic activity
    5a. Decreased para => decreased HR
    5b. Decreased sympa => decreased venomotor tone => increased venous volume => decreased EDV + decreased contractility => decreased SV + decreased HR => decreased CO + decreased TPR
  5. Decreased arterial pressure
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13
Q

How do baroreceptors respond to higher pressures?

A

Fire more frequently

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14
Q

Do baroreceptors only respond to blood pressure?

A

NOPE, they also respond to the pulse pressure in the same manner as with pressure (so even if the MAP is the same but the pulse pressure is getting wider, they can send signals)

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15
Q

In what range of pressures are the baroreceptors sensitive?

A

60 to 160 mmHg MAP

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16
Q

What happens to the baroreceptor reflex when you have chronic hypertension?

A

They will adapt and fire less in the normal range => shift to a higher range of pressures at which they are sensitive

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17
Q

Through what curve do we represent the baroreceptor reflex? What does chronic HT do to this curve? Why?

A
  • X-axis = Arterial BP
  • Y-axis = Number of impulses from carotid sinus per second

=> sigmoidal cuve

Chronic HT = shift to the right so that the reflex can keep the pressure constant rather than have it constantly go up and down

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18
Q

Does the medullary CV center only receive input from peripheral baroreceptors? Example?

A

NOPE, also from other areas of the brain

E.g. explains how we can faint from fear

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19
Q

Does the sympathetic NS extends to all vessels of the body?

A

YES, with some exceptions:

  1. Thoracic aorta
  2. Brain arteries and veins
  3. Capillaries (no smooth muscle)
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20
Q

What vessels does the parasympathetic NS innervate? Through what nerves?

A
  1. Lower GIT vessels
  2. Urogenital organ vessels

Through pelvic splanchnics of the sacral spinal cord (S2-S4)

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21
Q

Compare the sympathetic effects on the arteries vs veins.

A
  1. Arteries: focal stimulation on capillary beds to increase TPR because large arteries cannot be efficiently constricted by SNS and because in some tissues metabolic vasodilation will take over
  2. Veins: overall constriction of the reservoir to decrease their capacitance, increase venous pressure, and preload because veins all react in the same manner to SNS stimulation
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22
Q

What hormone will the adrenal medulla release upon sympathetic activation?

A

EPI

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23
Q

What are the effects of sympathetic stimulation on a particular tissue?

A
  1. Increased arteriolar resistance => reduced flow

2. Increased venous constriction => reduced venous capacitance => reduced tissue volume

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24
Q

To which adrenergic receptors does NE bind to?

A
  1. Beta1

2. Alpha1

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25
Q

To which adrenergic receptors does EPI bind to?

A
  1. Beta1
  2. Beta2
  3. Alpha1
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26
Q

What 3 types of adrenergic receptors work to regulate flow to skeletal muscles depending on activity? Which one is the major player?

A
  1. Alpha adrenergic activated to reduce blood flow***
  2. Beta2 receptors activated to increase blood flow
  3. Atypical sympathetic cholinergic receptors activated to increase blood flow (some sympathetic nerves actually release ACh)
27
Q

Do sympathetic nerves only release catecholamines?

A

NOPE

28
Q

What do complex physiological states require?

A

Complex regulation of the vascular system via the very complex ANS

29
Q

What are cardiopulmonary baroreceptors? How do they work?

A

Low pressure mechanoreceptors located in the atria of the heart and pulmonary great vessels (both low pressure environments)

=> detect changes in BV by stretching in response to increase BV => send signals to medullary CV center => inhibition of release of ADH by pit + opposing effects on 2 sympathetic tracts to reduce BV:

  1. Sympathetic tract to heart activated to increase HR to speed up blood distribution
  2. Sympathetic tract to kidneys inhibited to allow for vasodilation to increase blood flow = increased urine production to decrease BV
30
Q

What is ADH? Function?

A

Antidiuretic hormone:

  1. Water re-absorption by the kidney to increase BV and reduce blood osmolality
  2. Direct vasoconstriction, which is only relevant to BP regulation in pathophysiological states (shock, dehydration)
31
Q

Medical term for urine production?

A

Diuresis

32
Q

How are inputs to the medulla integrated? E.g.?

A

High and low baroreceptors’ and chemoreceptors’ input are integrated in the medullary CV center to ensure that the correct adaptive response ensues

E.g. to make sure signals received by low P baroreceptors are not caused by transient volume increases due to position shifts, the medulla should also receive high BP signals from the high P baroreceptors

33
Q

In what nerve are the cardiopulmonary baroreceptor afferents found?

A

Vagus nerve + sympathetic afferents

34
Q

Describe the regulation of the HR via peripheral chemoreceptors.

A

Chemoreceptors in aortic arch and carotid sinus that detect the quality of the arterial blood: PO2, PCO2, pH levels

35
Q

Describe the mechanisms of the regulation of HR via peripheral arterial chemoreceptor reflex.

A

High PCO2/Low CO2/Low pH:

  1. Primary effect: chemoreceptors send signals to the medullary CV center to decrease HR and increase SNS activity to redirect blood flow to the brain (survival mode)
  2. Secondary effect: due to chemoreceptors sending a signal to the lungs and causing hypocapnia and increased lung stretch => inhibition of the medullary CV center to stop it from decreasing HR and make it go back to normal (bradycardia is transient if respiration is successfully increased)
36
Q

How do central chemoreceptors work?

A

Brain chemoreceptors detect the quality of arterial blood mainly via the CO2 levels to increase or decrease blood flow to itself

37
Q

What is the main goal of humoral mechanisms? Is this important for moment-to-moment regulation of BP?

A

Regulation of fluid/blood volume and electrolyte levels for LONG-term BP regulation

NOPE, it is not UNLESS there there is a crisis like a massive hemorrhage

38
Q

Describe the Renin-Angiotensin-Aldosterone (RAA) system.

A

Low BP/Low fluid volume => decreased stretch of cardiopulmonary baroreceptors => signals to medulla decreased => increased beta1 sympathetic stimulation on kidneys => increased secretion of renin by kidneys => renin converts angiotensinogen produced by the liver to angiotensin I => ACE in endothelium converts angiotensin I to II => angiotensin II causes 3 effects:

  1. Adrenal glands secretion of aldosterone
  2. Vasoconstriction
  3. NaCl/H2O reabsorption by the kidneys
39
Q

What is angiotensinogen?

A

A plasma protein

40
Q

Action of aldosterone?

A

Na+/H2O reabsorption by the kidney (and K+ excretion)

41
Q

What is renin?

A

A peptide enzyme

42
Q

Where is ACE mostly found?

A

Endothelium of the lungs

43
Q

Can the vasoconstriction by angiotensin II actually increase BP in the short-term?

A

Not throughout the body no, not enough it released, but it can have a role in pathophysiologic states such as hemorrhagic shock

44
Q

What does one molecule being a secretatogue for another mean?

A

Causes the secretion of it

45
Q

What can excessive activation of the RAA system cause?

A

Runaway HT

46
Q

Describe the release and modes of action of atrial natriuretic peptide.

A

Atrial myocytes stretch and function as mechanoreceptors => release ANP in bloodstream:

  1. Increased kidney natriuresis (= excretion of Na+) and diuresis
  2. Vasodilation of renal arteries
  3. Inhibits the release of aldosterone by the adrenal medulla
47
Q

Do the vasodilatory effects of ANP extend beyond the renal arteries?

A

NOPE

48
Q

Is the heart an endocrine hormone?

A

YUP

49
Q

What 2 factors can cause ADH release by the pit?

A
  1. Decrease in BV

2. Increase in blood osmolality

50
Q

Other name for ADH?

A

Vasopressin

51
Q

What are 3 other humoral factors in the regulation of the CV system?

A
  1. Endothelin
  2. Epinephrine
  3. Various inflammatory mediators and platelet products
52
Q

What is the effect of various inflammatory mediators and platelet products in the regulation of the CV system?

A

Local effects on vascular tone but no physiological role in BP regulation

53
Q

What is the gain of a regulatory mechanism?

A

Measure of the level of response for a given signal

54
Q

What is the order of regulatory mechanisms kicking in in response to hemorrhage? Also rate they maximum feedback gain in response to optimal stimulation.

A
  1. Baroreceptor reflex (3)
  2. Chemoreceptor reflex (4)
  3. CNS ischemic response (2)
  4. RAA system (1)
55
Q

What is short-term BP control largely dependent on?

A

Neural feedback pathways of baro and chemoreceptors

56
Q

What is long-term BP control largely dependent on?

A

Mechanisms that restore BV through humoral renal effects

57
Q

Compare the physiologic and pharmacologic effects of mediators of the CV system.

A

Pharmacological effects of the same substances than those produced by our bodies can have different effects due to different (patho)physiological contexts and feedback responses.

58
Q

What is the physiological response to an EPI infusion?

A
  1. Binding to beta1: increased SV/HR/contractility = increased CO
  2. Binding to alpha1: decreased venous capacitance = increased CO + on kidneys/skin: decreased flow
  3. Binding to beta2: increased flow to splanchnics and muscles = decreased TPR

OVERALL => unchanged MAP and increased pulse pressure (increase in systolic due to CO/decrease in diastolic do to TPR)

59
Q

What is the physiological response to an NE infusion?

A
  1. Binding to alpha receptors on all organs (even muscles because not in a sympathetic state) = decreased flow and increased TPR
  2. Binding to beta1 receptors: increased SV/contractility = unchanged CO due to increased TPR
  3. Binding to alpha1: decreased venous capacitance = unchanged CO due to increased TPR

OVERALL => increased BP => baroreceptor reflex => decreased HR

60
Q

Can the SNS constrict all of the veins and none of the arteries?

A

NOPE

61
Q

Would the medulla be able to only activate certain sympathetic or parasympathetic nerves?

A

Yes, 2 examples:

  1. Chemoreceptor reflex activates SNS vasoconstriction of all vessels and inactivates SNS stimulation on heart
  2. Cardiopulmonary baroreceptors in response to increase in BV cause activation of SNS stimulation on heart and inactivation of SNS vasoconstriction of kidney vessels so that they can filter more blood for diuresis
62
Q

Does the adrenal medulla only release EPI upon sympathetic stimulation? Not NE?

A

It does, but 6:1 ratio

63
Q

Why is there more parasympathetic activity on heart at rest than SNS?

A

Because parasympathetic allows for very short-lived moment to moment regulation so it’s more appropriate

SMP - Cardiopulmonary Exam 1 (28 decks)

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