Hormonal Control of Blood Pressure Flashcards

1
Q

Integrated systems regulate MAP

A
  • when hemorrhage causes a sudden decrease in arterial pressure, the pressure control system faces 2 challenges: 1st- respond rapidly enough to ensure survival; 2nd- gradually reestablish blood volume to normal levels
  • they are accomplished by integrated actions of systems that respond rapidly (sec - min); intermediate (min-hrs); and long term (days or longer)
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2
Q

Rapid acting control mechanisms

A
  • typically nervous reflexes

- the baroreceptors, chemoreceptors, and CNS ischemic response

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3
Q

Intermediate control mechanisms to regulate MAP

A
  • include the renin-angiotensin vasoconstrictor mechanism, the stress relaxation mechanism (e.g. increased pressure for min-hrs leads to continuous stretch of the vessel to relieve the pressure
  • capillary fluid shift mechanism (e.g. if capillary pressure falls too low, fluid is fluid is absorbed from the tissues through the capillary membranes thus building up blood volume and pressure
  • during this time, nervous mechanisms become gradually less effective
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4
Q

Long term control mechanisms to regulate MAP

A

-involves control by the kidneys, in particular the renin-angiotensin-aldosterone system

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5
Q

CNS ischemic response

A
  • when blood flow to the vasomotor center in the lower brain stem becomes decreased enough to cayse ischemia- the vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond directly to ischemia and become strongly excited
  • this arterial pressure elevation in response to cerebral ischemia is known as the CNS ischemic response
  • one of the most powerful of all the activators of the sympathetic vasoconstictor system
  • it does not become significant until the arterial pressure falls far below normal, down to 60 mm Hg, and to greatest degree 15-20 mm Hg
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6
Q

High pressure baroreceptors

A

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

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7
Q

Low pressure baroreceptors

A
  • decerase their firing rate in response to decreased circulating volume
  • this leads to increased SNS mediated vasocontriction, especially the renal bed (they also stimulate ADH release)
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8
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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9
Q

Central chemoreceptors

A

-respond to brain ischemia (a fall in pH/acidosis) leading to a powerful SNS output (the kidney can actually stop producing urine)

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10
Q

Angiotension II

A

-decreased arterial pressure -> renin (kidney) -> renin substrate (angiotensinogen) -> angiotensin I -> (by converting enzyme in lung ACE ) angiotensin II -> angiotensinase inactive, vasoconstriction, renal retention of salt and water -> increased arterial pressure

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11
Q

Recovery from hemorrhage with angiotensin

A
  • hemorrhage causes arterial pressure to drop from 100 mm Hg to 50 mm Hg, the renin-angiotensin vasoconstrictor response is powerful enough to return pressure back to ~83 mm Hg
  • this response can be life-saving, especially in circulatory shock
  • in the presence of renin-blocking antibody recovery was much weaker returning to 60 mm Hg
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12
Q

Integrated responses to hemorrhage

A
  • response to hemorrhage involves contributions of the baroreceptors, the renin-angiotensin-aldosterone system, as well as increased fluid reabsorption by the capillaries in response to a decrease in capillary hydrostatic pressure
  • the unstressed volume refers to the volume of blood that the veins can hold, no pressure
  • the stressed volume refers to the volume in the arteries. This volume of blood produces pressure by stretching the elastic fibers in the walls of the vessels
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13
Q

Increased salt intake

A

-increased salt intake -> increased extracellular volume -> increased arterial pressure -> decreased renin and angiotensin -> decreased renal retention of salt and water -> return of extracellular volume almost to normal -> return of arterial pressure almost to normal

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14
Q

Antidiuretic hormone (ADH; vasopressin)

A
  • from the posterior pituitary function, synthesized in the supraoptic nuclei of the hypothalamus and stored and released in posterior pituitary
  • main function is water balance; it is released in response to increase osmolarity of extracellular fluid and decreased blood pressure and has the major effect of promoting water reabsorption by the kidney.
  • high ADH in plasma, a low volume of concentrated urine is produced
  • vasopressin/ADH is also a vasoconstrictor
  • released in response to increased body fluid osmolarity, decreased blood volume, and decreased blood pressure
  • ANP (atrial naturetic peptide), ethanol, aldosterone decreases release
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15
Q

Control of arteriolar tone

A
  • greatest resistance to flow occurs in the small arteries and arterioles
  • the state of construction of relaxation of these vessels is regulated in part by the sympathetic nervous system and release of norepinephrine
  • circulating hormones, including ADH, angiotensin, may contribute to constriction through their actions on vascular smooth muscle; atrial natriuretic peptide (ANP) is a smooth muscle dilator
  • endothelium plays an important role in regulating vascular tone by its release of NO and prostacycline in response to shear stress, ACh, and bradykinin
  • endothelin is a potent, endothelium-derived vasoconstrictor important in some pathophysiologic states
  • the endothelial cell surface also has angiotensin-converting enzyme (ACE), which forms angiotensin II by cleavage of circulating angiotensin I
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16
Q

Integrated systems regulate MAP both acutely and chronically

A
  • to maintain adequate blood flow to tissues, the body has a complicated system for monitoring and regulating blood pressure
  • high pressure baroreceptors in the aortic arch and carotid sinus are extremely important in acute regulation of blood pressure, through their effects on the ANS
  • afferent arterioles in the renal juxtaglomerular apparatus also contain high pressure baroreceptors; these are involved in regulation of renin release, and consequently, regulation of sodium and water balance, important in long term regulation of blood pressure
  • low pressure baroreceptors in the heart and pulmonary circulation respond to changes in blood volume and modulate sympathetic activity and vasopressin release
  • the cardiac atria also release atrail natriuretic peptide in response to elevated blood volume
17
Q

Long term response to changes in blood volume and pressure

A
  • in addition to evoking mechanisms for acute adjustment of blood pressure, changes in blood volume and pressure will also activate renal mechanisms for adjusting blood volume
  • reduced blood volume and therefore arterial pressure will stimulate the renin-angiotensin-aldosterone system, with the end result of sodium and water retention
  • reduced BP will also activate sympathetics stimulates renin secretion and have direct effects on kidneys
  • increased volume will stimulate ANP release by heart. ANP has direct renal effects (natriuresis and diuresis) and also inhibits aldosterone release by the adrenal medulla