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Cardiovascular physiology > Final exam > Flashcards

Final exam Flashcards

1
Q

Neurotransmitter release is proportional to what?

A

Nerve stimulation frequency

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2
Q

What is NT release subject to?

A

Neuromodulation

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3
Q

What do Alpha 2 adrenergic receptors on the nerve varicosity do when stimulated by Norepi release?

A

Decrease subsequent neurotransmitter release

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4
Q

What receptors for metabolites and other vasoactive substances decrease neurotransmitter release?

A
  • K+
  • Adenosine
  • PGE1
  • Histamine
  • S-HT
  • ACH
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5
Q

What receptor for metabolites or other vasoactive substance increases NT release?

A

Angiotensin 2

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6
Q

What do sympathetic vasoconstrictor nerves also release with NT?

A

ATP and NPY

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7
Q

What does ATP do when released from sympathetic vasoconstrictor nerves?

A

Contributes to smooth muscle cell depolarization

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8
Q

What does NPY do when released from sympathetic vasoconstrictor nerves?

A
  • Causes slow, prolonged depoarization of SMC

- Sensitizes SMC to norepi

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9
Q

When is NPY released from sympathetic vasoconstrictor nerves?

A

in response to high frequency stimulation (stress)

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10
Q

What vessels are most innervated with sympathetic vasoconstrictor nerves?

A

Arteries and large arterioles

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11
Q

What vessels have poor innervation by sympathetic vasoconstrictor nerves?

A
  • Veins
  • Smallest arterioles
  • Cerebral arteries
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12
Q

What is the exception to poor venular innervation by sympathetic vasoconstrictor nerves?

A

veins in skin and splanchnic region are innervated (important for venoconstriction in these regions)

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13
Q

Are sympathetic nerves tonically active?

A

yes

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14
Q

Where do sympathetic nerves contribute to resting tone?

A

In many vascular beds

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15
Q

How is sympathetic stimulation regulated in vascular beds?

A

Each has its own independent sympathetic input represented by a specific region of the ventrolateral brainstem

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16
Q

When may all sympathetic neurons be activated?

A

During extreme responses (e.g. hemorrhage)

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17
Q

What is released from the adrenal medulla with sympathetic stimulation?

A

epinephrine and norepi

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18
Q

What is adrenal secretion stimulated by?

A
  • Intense exercise
  • Fear
  • Hypotension
  • Hypoglycemia
  • Hemorrhage
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19
Q

What does epinephrine stimulate in the liver?

A

Glycogenesis

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20
Q

What does epinephrine stimulate in adipose tissue?

A

lipolysis

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21
Q

What does epinephrine do to beta 1 adrenergic receptors?

A

acts on them to increase heart rate and contractility

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22
Q

What does epinephrine do in skeletal muscle, myocardium and liver?

A

Causes vasodilation

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23
Q

Why does epi cause vasodilation in skeletal muscle, myocardium and liver?

A

Abundance of beta 2 adrenergic receptors

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24
Q

Which receptors does epi have a greater affinity for?

A

Beta adrenergic

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25
Q

Which receptors does norepi have a greater affinity for?

A

Alpha adrenergic

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26
Q

What would a injection of norepi into a human do?

A

Increase total peripheral resistance due to wide-spread activation of alpha adrenergic receptors

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27
Q

What would a injection of epi into a human do?

A

Slight decrease in total peripheral resistance due to activation of beta 2 adrenergic receptors in large mass of skeletal muscle counterbalanced by activation of alpha adrenergics in other tissues

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28
Q

What do both nor epi and epi do when injected into the body?

A

Increase heart rate and cardiac contractility by stimulation of cardiac beta 1 adrenergic receptors

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29
Q

What are sympathetic vasodilator nerves in skin called?

A

Sudomotor-vasodilator cholinergic fibers

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30
Q

What do sympathetic vasodilator nerves in the skin release

A

Acetylcholine and probably VIP

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31
Q

What do sympathetic vasodilator nerves in the skin do?

A

Vasodilate skin arterioles and cause sweating

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32
Q

What kind of distribution do parasympathetic vasodilator nerves have?

A
  • Restricted distribution

- skin and muscle have no innervation form these

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33
Q

What are the pre-ganglyonic fibers of parasympathetic vasodilator nerves like?

A
  • Long and synapse within organ (release acetylcholine)

- Leave brain at vagus nerve and course down the spinal cord and leave the sacrum ( sacral spinal nerve)

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34
Q

What does the vagus nerve innervate?

A
  • Coronary arteries
  • Salivary glands
  • Exocrine pancreas
  • Gastrointestinal mucosa
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35
Q

What does the sacral spinal nerve innervate?

A
  • Genitalia
  • Bladder
  • Colon
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36
Q

Describe post-ganglionic fibers of parasympathetic vasodilator nerves.

A

Are within the end-organ and terminate on resistance arteries

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37
Q

What is the pathway of ACH when released by parasympathetic vasodilator nerves?

A

Primary neurotransmitter->binds to M2 receptors on EC-> Causes release of nitric oxide, EDHF, PGI2-> vasodilation

In some cells ACh binds to M3 receptor on SMC-> vasoconstriciton

38
Q

What does vasoactive intestinal peptide (VIP) and/or substance P do when released by parasympathetic vasodilator nerves?

A

VIP is predominant in pancreas

->both cause endothelium dependent vasodilation

39
Q

What does nitric oxide do when released by parasympathetic vasodilator nerves?

A
  • > some parasympathetic vasodilator nerves are “nitridergic”

- >found in resistance vessels of cerebrum, temporal lobe, mesentery, coronary, genitals

40
Q

What nerves are responsible for erection of genitalia?

A

Nitridergic nerves

41
Q

What does viagra (sildenafil) do?

A

Increases cGMP in arteries of genitalia, which causes vasodilation of the arteries and erection

42
Q

What PDE is sildenafil specific for?

A

PDE5

43
Q

What are nociceptive C-fibers?

A

sensory nerves

44
Q

What do nociceptive C-fibers control?

A

Local vasodilation to painful stimuli (not involved in MAP reg)

45
Q

What carries painful stimuli to the brain?

A

Nociceptive C-fibers

46
Q

What do C-fiber collaterals do?

A

Innervate blood vessels and sometimes mast cells

47
Q

What does vasodilation of local blood vessels by Nociceptive C-fibers do?

A

Causes area of redness, swelling around the injured site (flare) mediated by CGRP

48
Q

When is RAAS elevated?

A

In essential hypertension and cardiac failure

49
Q

What are the three effects of chronically elevated angiotensin 2?

A

1) enhances platelet aggregation
2) stimulates cardiac hypertrophy (with fibrosis
3) Stimulates inward remodeling and increased wall thickness in arteries

50
Q

Vasopressin (AVP or antidiuretic hormone) are released from the hypothalamus in response to what?

A
  • Increased plasma osmolality

- Decreased MAP or blood volume

51
Q

What chain effects does Atrial natriuretic peptide do?

A

Increased atrial pressure-> Myocytes within atria release ANP-> Increased salt and water excretion by kidney, mild vasodilation, and decreased venular permeability which leads to interstitial volume increase-> Decreased MAP

52
Q

What can increase atrial natriuretic peptide levels two fold?

A

Water immersion

53
Q

What can increase atrial natriuretic peptide levels twenty fold?

A

Heart failure

54
Q

What does insulin do?

A
  • Increase NO

- Decrease SMC growth (anti-atherogenic)

55
Q

What does estrogen do?

A

Increase NO by activating eNOS

-Increases eNOS expression

56
Q

What does relaxin do?

A

Causes vasodilation in uterus, mammary gland, and heart during pregnancy and delivery

57
Q

Where is relaxin secreted from?

A

Corpus luteum of ovary

58
Q

What does thyroxin (T4) do?

A
  • Increase cardiac contractility by increasing Beta1-adrenergic receptor expression
  • Increase metabolic rate which causes vasodilation
59
Q

Where are cardiovascular baroreceptors mainly found?

A
  • Arterial

- Cardiopulmonary

60
Q

Where are cardiovascular chemoreceptors found?

A
  • Aorta

- Carotid

61
Q

Where are cardiovascular mechanoreceptors found?

A

Muscle

62
Q

How is acute regulation of MAP controlled?

A

Control of heart and blood vessels

63
Q

How is chronic regulation of MAP controlled?

A

Control of plasma volume

64
Q

Where are baroreceptor nerve endings found?

A

Adventitia of arteries

65
Q

Where do baroreceptor afferents travel to?

A

The nucleus tractus solitarius (NTS) in the brainstem

66
Q

What do baroreceptors detect?

A
  • Distension of the blood vessel wall

- Both static stretch and rate of change

67
Q

Describe the A-fiber type of baroreceptor afferent.

A
  • Large diameter
  • Fast conducting
  • Myelinated
  • Low threshold
  • High sensitivity
  • Detect primarily normal pressure ranges
68
Q

Describe the C-fiber type of baroreceptor afferents.

A
  • More abundant
  • Narrow, slow conducting
  • Unmyelinated
  • High threshold
  • Low sensitivity
  • Detect high pressures
69
Q

What two pressures do baroreceptors detect?

A

Mean and pulse

70
Q

What does increased MAP do to baroreceptor firing?

A

Recruits more afferents to fire

71
Q

What difference is there between afferent firing rate during pulsatile pressure vs steady pressure?

A

Higher firing rate during pulsatile, even though mean pressure is same

72
Q

When is baroreceptor afferent firing rate important?

A

During orthostasis and moderate hemorrhage

73
Q

What happens if NTS is destroyed?

A

Hypertension

74
Q

What are arterial baroreceptors responsible for?

A

Baroreflex

75
Q

What does baroreflex do?

A

-Acute adjustments in heart rate, contractility and vascular tone to regulate MAP

76
Q

What is baroreceptor firing proportional to?

A

MAP

77
Q

What is baroreflex central resetting?

A

Inputs from higher centers or other receptors can shift baroreflex curve upward

78
Q

What does “central command” (signals from cerebral cortex) do in baroreflex re-setting?

A

Stimulates the brainstem to increase sympathetic nerve activity

79
Q

What do receptors from working muscle do in baroreflex re-setting?

A

Stimulate sympathetic nerve activity via the NTS

80
Q

What is peripheral baroreflex resetting?

A

Sustained increase in MAP (>15min) causes an upward shift in the baroreflex curve, and it is then regulated around a new set-point

81
Q

Because of peripheral re-setting, baroreflex primarily controls what?

A

Acute fluctuations in MAP (buffers MAP around a set point)

-Cannot control long term MAP

82
Q

What happens to MAP if arterial baroreceptors are cut or damaged?

A

MAP is unstable with wide fluctuation

  • Large increase with exercise at abou 5x
  • first could of days after it happens MAP significantly elevated
  • After a few days only slightly elevated but still wide fluctuations throughout the day
83
Q

What causes myelinated venoatrial mechanoreceptors to fire?

A

Fire in response to expansion of the heart so they are sensitive to changes in CVP and cardiac filling

84
Q

What path do the myelinated venoatrial mechanoreceptor fibers take?

A

Travel up vagus nerve to the NTS

85
Q

What do myelinated venoatrial mechanoreceptors do once they are activated?

A
  • Provoke tachycardia by selective activation of SNA with no change in PNA
  • Provoke diuresis (Decrease renal SNA, vasodilate renal arteries and arterioles, decrease volume preserving hormones, increase ANP)
86
Q

How abundant are non-myelinated mechanoreceptors and chemoreceptors?

A

More abundant than myelinated fibers (~80% of cardiopulmonary receptors)

87
Q

When do non-myelinated mechanoreceptors fire?

A

When heart is overdistended, travel up vagus to NTS and cause decrease in HR and slight vasodilation

88
Q

What do nonmyelinate chemoreceptors do?

A

Sense pain associated with ischemia (angina) and converge with central sensory tract

89
Q

What would happen if all cardiopulmonary afferents were cut or destroyed?

A

Bothe MAP and HP would be chronically elevated

90
Q

What would happen if cardiopulmonary afferents were selectively stimulated?

A

HR would decrease, vasodilation, hypotension

91
Q

What do arterial baroreceptors do?

A

Buffer changes in MAP

92
Q

What do cardiopulmonary baroreceptors do?

A

Sense changes in central blood volume

Cardiovascular physiology (3 decks)

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