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Cardiovascular I > Central Neural and Humoral Control of Blood pressure > Flashcards

Central Neural and Humoral Control of Blood pressure Flashcards

1
Q

What is the over all effect of the sympathetic N.S. on TPR?

A

Increases

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2
Q

Vasoconstrictor sympathetic fibers are widely dispersed, where are they most/least concentrated?

A

Most: Kidney and skin

Least: heart and brain

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3
Q

•Norepinephrine:

Adrenoceptors on VSMC -> generalized vasoconstriction (pressor effect)

The exceptions include?

A

•Exceptions include skeletal and cardiac m. response can promote vasodilation (β2 )

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4
Q

What is the primary neural influence on arteriolar smooth muscle?

Via what receptors and NT’s is this accomplished?

A

Sympathetic

Vasoconstriction:

α₁ receptors: Norepinephrine, epinephrine

Vasodilation
β₂ receptors preferentially bind epinephrine (expression: skeletal m., cardiac m., liver, & adrenal medulla

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5
Q

What are the five components of the negative feedback loop involved in neural reflexes?

A
  1. Receptor
  2. Afferent path
  3. integration center
  4. efferent path
  5. effector
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6
Q

What are the receptors involved in MAP regulation?

A

Baroreceptors

Chemoreceptors

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7
Q

What types of baroreceptors are there? What do they detect?

A

mechanoreceptors, detect stretch

–High-pressure receptors
–Low-pressure receptors

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8
Q

What do chemoreceptors detect?

A

detect changes in blood PO2, Pco2, [H+]

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9
Q

What is the primary integration center involved in MAP regulation?

A

medulla oblongata; cerebral cortex & hypothalamus

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10
Q

What are the 4 effectors of MAP regulation?

A

–Cardiac myocytes (pacemaker & contractile)
–Arterial & venous vascular smooth muscle cells (VSMCs)
–Adrenal medulla
–Kidneys

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11
Q

What six things provide feedback to the medulla oblongata?

A

–Baroreceptors
–Chemoreceptors
–Hypothalamus
–Cerebral cortex
–Skin
–Local CO2 and O2 concentrations

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12
Q

What are the most important high-pressure baroreceptors?

A

Carotid sinus and aortic arch

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13
Q

What does an increased receptor stretch due to increased pressure lead to regarding high pressure receptor firing rate?

A

Increases it.

(graded response with amplitude proportional to amount of stretch)

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14
Q

Outline the 8 steps of the high-pressure baroreceptor reflex response to increased MAP.

(Important)

A
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15
Q

Baroreceptors respond to increased MAP by causing vasodilation and decreased heart rate. Describe how this is accomplished beginning with the stretch sensation

A

TPR
–↑ Baroreceptor stretch
–↑ Baroreceptor firing rate
–Inhibition of vasomotor area
–↓ Sympathetic output
–↓ vasoconstriction
–↑ Vasodilation

HR

–↑ Baroreceptor stretch
–↑ Baroreceptor firing rate
–Excitation of interneurons in cardioinhibitory area
–↑ Parasympathetic output
–↓ Heart Rate

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16
Q

Which baroreceptors predominate?

What kind of pressure to these mostly respond to?

A
  • Carotid baroreceptors predominate over aortic
  • Greater response to pulsatile vs. steady pressure
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17
Q

What are the low-pressure baroreceptors? Where are they found? What do they regulate?

A

Cardiopulmonary receptors:

  • In cardiac chambers and large pulmonary vessels
  • Involved in blood volume regulation
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18
Q

What do the A and B fibers of the low pressure baroreceptors monitor respectively?

A

•A fibers: monitor HR (fire during atrial systole)
B fibers: monitor atrial volume

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19
Q

What is the response of increased low pressure baroreceptor firing rate? (on heart rate and renal vessels)

A

Reflex Response:

•↑ HR•↓ Renal vasoconstriction

(Promotes renal vasodilation)

–↑ Renal blood flow
–↑ Urine output
–↓ Effective circulating volume

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20
Q

What does the bainbridge reflex do?

A

Counterbalances the high-pressure baroreceptor reflex

  • ↑stretch of high-pressure receptors → ↓ HR
  • ↑stretch of low-pressure receptors → ↑ HR
  • High-pressure baroreceptors: generalized vasodilation
  • Low-pressure baroreceptors: renal vasodilation
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21
Q

At what point in the cardiac cycle is the bainbridge reflex dominant?

A

During volume loading

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22
Q

During which point of the cardiac cycle is the high pressure baroreceptor reflex dominant?

A

volume depletion

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23
Q

At low blood volume, what impact does the baroreceptor reflex have on the slope of the starling relationship?

A

•Baroreceptor reflex

↑ sympathetic output ->↑ contractility & slope of Starling relationship

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24
Q

At high blood volume what impact does the baroreceptor reflex have on the starling relationship?

A

•↓ sympathetic output -> ↓ contractility & plateau of Starling relationship

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25
Q

What are the peripheral chemoreceptors? Where are they located?

A

•Carotid body (carotid a. bifurcation)

Aortic bodies (aortic arch)

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26
Q

What do peripheral chemoreceptors do?

A

Detect changes in arterial blood

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27
Q

What does the chemoreceptor reflex do?

A

–Primarily regulates respiration

(increased rate and depth)
–Some influence on cardiovascular system

(vascular tone and HR)

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28
Q

What is the chemoreceptor integrated physiologic response?

A

Vasoconstriction and tachycardia

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29
Q

If ↓ MAP and ↑ Pco2 ↓ pH ↑ [H+] occur simultaneously, what happens?

A

•↑ stimulation of chemoreceptors and ↓ stimulation of baroreceptors -> ↑ vasoconstriction

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30
Q

If ↑ Pco2 ↓ pH ↑ [H+] occurs along with ↑ MAP

A

•↑ stimulation of chemoreceptors and ↑ stimulation of baroreceptors -> (ex: high carotid sinus pressure and low Pao2) -> baroreceptor-mediated inhibition of vasoconstriction dominates

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31
Q

What are the major hormones that control vascular resistance?

4

A
  • Epinephrine
    - Angiotensin II (ANG II)
    • Atrial natriuretic peptide (ANP)
  • Anti-diuretic hormone (ADH) = Arginine Vasopressin (AVP, Vasopressin)
32
Q

What are the hormones that control blood volume?

3

A

Anti-diuretic hormone (ADH) = Arginine Vasopressin (AVP, Vasopressin)

  • Aldosterone
  • Atrial natriuretic peptide (ANP)
33
Q

What hormone controls heart rate and stroke volume?

A

Epinephrine

34
Q

Where is epinephrine produced? What does it do when binding alpha 1 and beta 2 receptors respectively?

A

adrenal gland

  • Vasoconstriction via α₁, vasodilation via β₂ receptors
35
Q

What is ANG I converted to ANG II by? What does it do? What is it stimulated by? Where is it released?

A

Converted from ANG I by ACE (mainly in lungs; ACE is secreted by pulmonary and renal endothelial cells)

  • Vasoconstriction
  • Ex: released during blood loss or exercise
  • ↓renal BP à stimulates renin release
36
Q

What is the effect of ADH/AVP that is released by the posterior pituitary? When is it released?

A

Vasoconstriction

  • Ex: released during hemorrhagic shock
37
Q

Histamine is released in response to tissue trauma, what is the result of this?

A

Vasodilation (arteriolar), Venoconstriction

38
Q

Atrial myocytes release ANP, what does this lead to?

A

Vasodilation

39
Q

Characterize the response time of endocrine control of blood volume

A

Long-term

40
Q

What is the key effector organ for long term blood volume regulation? How does it regulate this?

A

Kidney

–Regulation of Na+ and H2O excretion in urine

41
Q

What are the 3 humoral regulators of blood pressure?

A
  1. Renin Angiotensin Aldosterone System (RAAS)
  2. Antidiuretic Hormone (ADH)/Vasopressin (AVP)
  3. Atrial Natriuretic Hormone (ANH/ANP)
42
Q

Review the renin-angiotensin-aldosterone system on slide 70. Draw it.

A
43
Q

What are the major effects of angiotensin II? (6)

A
  1. Vasoconstriction
  2. Stimulates adrenal gland aldosterone production
  3. Stimulates ADH/AVP
  4. Stimulates thirst
  5. Stimulates renal Na+ reabsorption
  6. Stimulates SNS activity
44
Q

What triggers secretion of aldosterone by the adrenal cortex? What does it promote?

What does this do to MAP?

A

ANG II

  • Promotes renal Na+ reabsorption
  • H2O follows by osmosis
  • ↑ Effective Circulating Volume•↑ MAP
45
Q

If the hypothalamus detects increased osmolarity, what does it do?

A

Stimulate fluid retention by increased release of vasopressin (and ANGII) by the posterior pituitary gland. Leads to increased MAP

46
Q

What system does the atrial natriuretic peptide/hormone oppose?

A

renin-angiotensin-aldosterone system

47
Q

•Cardiac atrial cells (low-pressure baroreceptors) detect: ↑ wall stretch (↑ blood volume), what do they do in response?
What is the impact on MAP?

A
  • Secrete ANP (vasodilator AND natriuretic)
  • Results in ↓ renal Na+ reabsorption↑ Na+ excretion = natriuresis↑ H2O follows in urine

•↓ ECF volume, ↓ ECV, ↓ MAP

48
Q

Identify the neural and hormonal responses shown in the graph

A
49
Q

Understand the integrated response to a decreased effective circulating volume/MAP

Slide 80

A
50
Q

What is the dominant reflex responding to orthostatic changes?

What is the ANS response?

This leads to what regarding the muscle pump?

A

High pressure baroreceptor reflex responding to volume depletion.

•↑ Sympathetic; ↓ parasympathetic

Increased muscle pumping for increased venous return

51
Q

What is the vasovagal (vasopressor) syncope a common response to?

A

•sudden emotional stress, acute pain, sight of blood, etc.

52
Q

The vasovagal syncope response follows this pathway:

•(Vagal afferents) -> Higher CNS -> medulla oblongata:
–Dramatic ↑ parasympathetic output
– ↓ sympathetic output

What physiological changes result from this path?

A

•Bradycardia and hypotension
–↓ TPR, ↓ CO, ↓ MAP
Loss of consciousness: ↓ cerebral perfusion pressure

53
Q

In vasovagal syncope MAP decreases due to diminished TPR and CO, due to failure of activation of what response?

A

Baroreceptor Response

54
Q

What are the peripheral receptors and reflexes involved in the fight or flight response?

A

No peripheral receptors or reflexes

55
Q

How is blood flow to skeletal muscle increased in response to the fight or flight response?

A

•Adrenal medulla: epinephrine
–β2 adrenoceptor activation
–Vasodilation and ↑blood flow: skeletal m.
–If exercising: metabolite production also promotes vasodilation and ↑ flow via autoregulation

56
Q

During fight/flight, there is general vaso- and venoconstriction, how is this accomplished?

A

•Sympathetic output: norepinephrine & epinephrine
–α1 adrenoceptor activation
–↓ Renal and Splanchnic blood flow

57
Q

During F/F response how is cardiac output increased?

A

–↑ sympathetic and ↓ parasympathetic output
–↑ HR and ↑ SV (↑ contractility)

58
Q

During F/F response, how is blood volume maintained?

A

–↑ ADH/AVP -> ↓ urine output

59
Q

In F/F what causes the net increase in MAP?

A

–↑ CO
–Increase/decrease in TPR
•Depends on balance between vasodilation and vasoconstriction

60
Q

What are the central command changes in response to exercise?

How about local responses?

(Important)

A

Slide 95

61
Q

What organizes the early neural response in ANTICIPATION of exercise?

A

Hypothalamus

62
Q

What are the delayed responses to exercise?

A

•Mechanical response:
–Muscle pump
–Increased VR

•Chemical response:
–Autoregulation of exercising skeletal m.
–Metabolites -> vasodilation
–↓ TPR

63
Q

During exercise, what do muscle afferents and reflexes reinforce?

A

Sympathetic output

64
Q

What is the impact of exercising muscle on capillary hydrostatic pressure?

A

•Increased capillary hydrostatic pressure
–Arteriolar dilation
–Net fluid filtration
–↑ interstitial fluid hydrostatic pressure
•↑ lymphatic flow

65
Q

What is the increased O2 delivery during exercise due to?

A

•oxyhemoglobin dissociation relationship
–↓ pH
•Due to ↑ CO2 and lactic acid
–↑ temperature
–↓ Hb affinity for O2 , promotes “off-loading”

66
Q

By what factor can O2 consumption increase during exercise?

A

60x

67
Q

What are the 6 components of the integrated CV response during exercise?

A
  1. Exercise pressor reflex
  2. Sensitivity of baroreflexes
  3. Skeletal m. vasodilation
  4. Circulating epinephrine
  5. Venous return
  6. Temperature regulation
68
Q

Where does the exercise pressor reflex originate? What receptors mediate?

A

–Reflex originates within the exercising muscle -> Neural drive
•Stretch receptors: muscle tension
•Chemoreceptors: metabolites

69
Q

During exercise, we have continued sympathetic output despite increased MAP. How is this possible?

A

Arterial baroreflexes

–Re-set of arterial baroreflex sensitivity by central command

70
Q

Metabolites released locally dilate resistance vessels during exercise, to what degree is this possible?

A

20x

71
Q

Venous return increases during exercise, what causes this? What factors contribute to this balance?

A

–Muscle pump: ↑ VR à ↑ SV (Starling’s law) à ↑ CO
–Balance of SV, HR, Contractility, Relaxation rate

72
Q

What fibers maintain temperature regulation during exercise? How do they do it?

A

–Sympathetic cholinergic fibers activate to sweat glands

–Inhibition of sympathetic vasoconstriction to skin (constricted in early response) à↑ cutaneous flow

73
Q

How is stroke volume maintained in exercise induced tachycardia?

A
74
Q

What is the major cardiovascular component that decreases with exercise? What does this serve to offset?

A

MAP: General Increase

SBP > DBP

↑ PP

  • Due to increased CO
  • Offset by overall decrease in TPR
75
Q
A

Cardiovascular I (18 decks)

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