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Physiology Week 4 > Hormonal Control of BP > Flashcards

Hormonal Control of BP Flashcards

1
Q

integrated systems

A
  • CNS ischemic response
  • Baroreceptors
  • Chemoreceptors
  • Stress relaxation
  • caps
  • fluid shift
  • aldosterone
  • renal blood pressure volume control
  • must respond to sudden decrease and reestablish blood volume
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2
Q

rapidly responding

A
  • baro/chemo receptors

- CNS ischemic response

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3
Q

intermediate controls

A
  • renin-angiotensin vasoconstrictor mechanism
  • stress relaxation mechanism
  • capillary fluid shift mechanism
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4
Q

long term control

A
  • volume control by kidneys

- renin-angiotensin-aldosterone

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5
Q

CNS Ischemic Response

A
  • low levels of blood flow
  • concentration of CO2 increases
  • pH drops
  • arterial pressure elevation
  • high as 250 mmHg for several minutes
  • some vessels become totally occluded
  • only when pressure below 60, strongest at 15-20
  • cushing from increased pressure of CSF- cuts off flow and causes reactoin
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6
Q

four major groups of receptors

A
  • compensate for fall in MAP
  • high pressure baro
  • low pressure baro
  • peripheral chemo
  • central chemo
  • increase TPR and keep MAP near normal with moderate blood loss, CO stays down
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7
Q

high pressure baro

A

-decrease firing rate and increase HR, contractility, vasoconstriction

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8
Q

low pressure baro

A
  • decrease firing rate in response to decreased circulating volume
  • SNS mediated vasoconstriction increases, esp in renal bed
  • stimulate ADH
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9
Q

peripheral chemoreceptors

A

-respond to local hypoxia by increasing the firing rate of chemoreceptor afferents, leading to increased firing of SNS vasoconstrictor fibers and changes in ventilation

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10
Q

central chemoreceptors

A

-respond to brain ischemia leading to powerful SNS output

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11
Q

angtiotensin II

A
  • decreased arterial pressure
  • renin cleaves >
  • renin substrate (angiotensinogen) to
  • angiotensin I
  • converting enzyme from lung
  • angiotensin II-powerful and short acting vasoconstriction
  • renal retention of salt and water (via aldosterone), vasoconstriction–>increased arterial pressure
  • angiotensinase inactivates
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12
Q

recovery from hemorrhage

A
  • 100- 50 mm Hg
  • renin-angiotensin back to 83
  • without it, only to 60
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13
Q

integrated response to hemorrhage

A
  • baroreceptors, renin-angtiotensin aldosterone

- increased fluid reabsorption by caps in response to decrease in hydrostatic pressure

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14
Q

unstressed volume

A
  • volume of blood veins can hold

- no pressure

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15
Q

stressed volume

A

-in arteries

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16
Q

increased salt intake

A
  • increased ECF volume
  • increased arterial pressure
  • decreased renin and angiotensin
  • decreased renal retention of salt and water
  • return of ECF volume to almost normal
  • return of arterial pressure to almost normal
17
Q

ADH

A
  • contributes to MAP control
  • synthesized by supraoptic nuclei of the hypothalamus and stored and released at post pit
  • released in response to increased Osm of ECF (decreased volume) and decreased BP
  • promotes water reabsorption from kidney
  • ANP decreased the release of ADH
18
Q

arteriolar tone

A
  • greatest resistance in small arteries and arterioles
  • regulated by SNS
  • ADH and angiotensin II contribute to constriction
  • ANP dilates
  • endothelium releases NO and prostacyclin in response to shear stress, Ach, and bradykinin
  • endothelin
  • endothelial cell has ACE, makes angiotensin II
19
Q

monitoring BP

A

high P baro

  • afferent arterioles in the renal juxtaglomerular apparatus also contain high pressure baroreceptors
  • involved in renin release
20
Q

long term changes in blood volume and pressure

A
  • renal mechanisms
  • renin-angiotensin-aldosterone
  • sodium and water retention
  • reduced BP activates SNS, stimulates renin
  • increased vol will stimulate ANP, which inhibits aldosterone
21
Q

circulatory shock

A
  • compensated
  • progressive
  • end stage

Physiology Week 4 (6 decks)

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