hormonal control of BP Flashcards

1
Q

what are the 3 rapidly acting control mechanisms of MAP? and how fast do these act?

A

-baroreceptors
-chemoreceptors
-CNS ischemic response
seconds to minutes to act

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2
Q

what are the intermediate control mechanisms of MAP? (3) and how fast do these acT?

A

-renin angiotension vasoconstritcor mechanism
-stress relaxation mechanism
-capillary fluid shift mechanism
minutes to hours

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3
Q

what is the long term control of MAP? and how fast does this act?

A

-volume control by the kidneys (renin-angiotensisin-aldosterone system)
days or longer

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4
Q

when does the CNS ischemic response occur?

A

when there begins to be ischemia in the CNS

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5
Q

at what BP is CNS ischemic response stimulated, and when does it receive its maximum degree of stimulation?

A

activated at BPs below 60 mmHg

receives greatest amount of stimulation of a BP at 15-20 mmHg

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6
Q

what is the cushing reaction?

A

type of CNS ischemic response that results from increased pressure of the CSF around the vrain in the cranial vault

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7
Q

relating to the arterial blood pressure, when does the cushing reaction occur?

A

when the CSF pressure equals that of the arterial blood pressure

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8
Q

do the baroreceptor reflexts compensate for the primary disturbance causing the decrease in MAP?

A

NO!

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9
Q

what mechanisms compensate for the primary disturbance causing the decreased MAP?

A

thrist
transcapillary refill
renal conservation of salt and water

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10
Q

what are the 4 major groups of receptors that compensate for the fall in MAP?

A
  • high pressure baroreceptors
  • low pressure baroreceptors
  • peripheral chemoreceptors
  • central chemoreceptors
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11
Q

what is the low pressure baroreceptor’s response to decreased MAP?

A

decrease firing rate due to decreased circulating volume. Leads to increase SNS mediated vasoconstriction, especially in renal bed. They also stimulate ADH release

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12
Q

what is the high pressure baroreceptor’s response to decreased MAP?

A

decrease their firing rate leading to increased HR, cardiac contractility and vasoconstriction

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13
Q

describe the function of peripheral chemoreceptors

A

respond to local hypoxia by increasing firing rate of chemoreceptor afferents leading to increased firing of SNS vasoconstriction fibers and changes in ventilation

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14
Q

describe the function of central chemoreceptors

A

respond to brain ischemia (fall in pH) leading to powerful SNS output (kidney can stop producing urine all together)

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15
Q

baroreceptors and chemoreceptors together result in what?

A

increased TPR enough to keep MAP near normal with moderate blood loss (10-20%) but CO remains depressed

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16
Q

how long does renin circulate in the system?

A

30-60 minutes

17
Q

where is renin synthesized?

A

kidney in response to decreased MAP

18
Q

what is the function of renin?

A

if cleaves angiotensinogen to make angiotensin I

19
Q

what enzyme converts angio I to angio II?

A

ACE

20
Q

where is ACR located

A

in the endothelium of the lung vessels

21
Q

what is the function of ang II in the short term?

A

is is a short acting arterial vasoconstrictor

raises MAP by increasing TPR and promotes venous return to the heart by venoconstriction

22
Q

what is the function of ang II in the long term?

A
  • decreases renal excretetion of salt and water–slowly increases ECF volume and then artieral pressure
  • also acts on adrenal glad to release aldosterone
  • also promotes release of ADH/vasopression from posterior pituitary gland
23
Q

what does unstressed volume refer to?

A

volume of blood that veins can hold. produces no pressure

24
Q

what does stressed volume refer to?

A

the volume of blood that veins can hold

this produces pressure by stretching the elastic fibers in the walls of the vessels

25
Q

increased salt intake does what to renin-angiotension activity?

A

decreases it

26
Q

where is ADH synthesized?

A

hypothalamus in the supraopic nuclei. some in paraventricular nuclei

27
Q

where is ADH stored and secreted from?

A

pituitary gland

28
Q

what is the main function of ADH?

A

water balance

29
Q

list some conditions that will increase the release of ADH

A
  • increased body osmolarity
  • decreased blood volume
  • decreased BP
  • increased levels of ang II
  • pain/stress
  • nausea/vomiting (because it causes dehyration)
30
Q

what is the effect of atrial nautretic peptide on ADH?

A

it inhibits it

31
Q

where does the greatest resistance to flow occur?

A

in the arterioles and small arteries which are regulated by the SNS

32
Q

what is the effect of ANP on smooth muscle?

A

dilates it

33
Q

what is endothelin?

A

potent vasoconstrictor derived from the endothelium

34
Q

what types of substances will causes the endothelium to secrete N.O. and PG12

A

shear stress, acetylcholine and bradykinin

35
Q

what do the low pressure baroreceptors in the heart and pulmonary circulation do?

A

they respond to changes in blood volume and modulate sympathetic activity and vasopression (ADH) release

36
Q

if there is elevated blood volume in the atrium, what will it secrete?

A

atrial natiuretic peptide (ANP)

37
Q

what are the effects of ANP?

A

it has direct effects on the kidney (natriuresis and diuresis) and also inhibits aldosterone release by the adrenal medulla