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Flashcards in Hormonal Control of Blood Pressure Deck (22)
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what are the 3 rapidly acting control mechanisms?

nervous reflexes with immediate response (w/in seconds to minutes)
1. baroreceptors
2. chemoreceptors
3. CNS ischemic response


what are the 3 intermediate control mechanisms?

activate within minutes to hours
1. renin-angiotensin vasoconstrictor mechanism
2. stress relaxation mechanism (increased pressure leads to continuous stretch to relieve pressure)
3. capillary fluid shift mechanism (if pressure falls to low, fluid is absorbed from tissues to build up volume)


what is the long term control mechanism?

activates within hours to days, and can be infinitely high
volume control by kidneys, using the renin-angiotensin-aldosterone system


what is the most powerful activator of the sympathetic vasoconstrictor system? (hint: is rapidly acting)

CNS Ischemic response
-arterial pressure elevation in response to cerebral ischemia
-it doesn't become significant until MAP falls below 60 mmHg; most stimulated at 15-20 mmHg
-thus it is an emergency pressure control system (last ditch stand)


Cushing RXN

special type of CNS ischemic response from increased pressure to CSF around brain in cranial vault
-if CSF pressure rises up to MAP, could compress entire brain and cut off supply
-CNS ischemic response causes MAP to rise higher than CSF, so blood can flow again
-this also happens in hemorrhagic stroke when subarachnoid bleeding


what are the 4 main groups of receptors that compensate for falls in MAP after hemorrhage, and what do they do?

1. high pressure baroreceptors decrease firing rate to increase HR, cardiac contractility, and vasoconstriction
2. low pressure baroreceptors decrease firing rate to increase vasoconstriction (esp. in renal bed), stimulate ADH release
3. peripheral chemoreceptors increase firing rate due to hypoxia (and high CO2, low pH), increasing vasoconstriction and changes in ventilation
4. central chemoreceptors sense acidosis of brain ECF


what are the 4 receptors ultimately controlled by?

it's an integrated response orchestrated by the medulla


how is angiotensin II ultimately made?

decreased MAP triggers renin enzyme release from kidneys
-renin cleaves angiotensinogen (circulating PRO) to angiotensin I (weak vasoconstrictor, 10 AA)
-ACE converts AI into AII (powerful but short-acting arterial vasoconstrictor, 8 AA)


what are the actions of angiotensin II?

powerful but short-acting arterial vasoconstrictor
-raises MAP by increasing TPR, and promotes venous return to heart by causing venoconstriction
-important for long-term MAP control b/c decreases renal excretion of salt and water, increasing ECF volume and thus MAP
-acts directly on kidney to retain salt and water
-causes adrenal gland to release aldosterone to increase salt and water reabsorption by kidneys
-promotes release of ADH from posterior pituitary gland


how is angiotensin II inactivated?

by angiotensinases


recovery from hemorrhage with and without renin-angiotensin vasoconstrictor system

drop in MAP from 100 mmHg to 50 mmHg
-w/ RAS: brings pressure back to 83 mmHg after 15 minutes
-w/o RAS: weaker recovery, only up to 60 mmHg


how can the renin-angiotensin system be blocked?

with renin-blocking antibodies
-can no longer cleave angiotensinogen to angiotensin I


what is the control mechanism for fluid reabsorption by capillaries after hemorrhage?

reabsorption increases in response to a decrease in capillary hydrostatic pressure


unstressed VS stressed volume

unstressed - volume of blood the veins can hold, b/c despite large volume, veins exert no pressure
stressed - volume of blood in arteries that produces pressure by stretching elastic fibers in walls of vessel


3 stages of circulatory shock

1. compensated (body can fix it without outside intervention, such as donating blood)
2. progressive (body can recover if given medical treatment)
3. death (end stage; bleeding too much and compensation not enough; like the positive feedback from bleeding more than 2 liters)


effects of increased salt intake on renin-angiotensin activity

increased extracellular volume --> increased MAP --> decreased RAS --> decreased renal retention of salt and water --> return of ECV to normal --> return of MAP to normal


what stimulates ADH secretion?

-increased body fluid osmolality
-decreased blood volume or pressure
-antiogensin II
-nausea and vomiting


what inhibits ADH secretion?

-decreased body fluid osmolality
-increased body volume or pressure
-antrial natriuretic peptide


effects of ADH/(arg) vasopressin

made mainly in supraoptic/paraventricular nuclei of hypothalamus, stored in posterior pituitary
-released in response to increased osmolarity of ECF and decreased MAP
-promotes water reabsorption by kidney
-when ADH levels are high, low volume of concentrated urine is produced


effects of atrial natriuretic peptide

released in response to increased blood volume
-decreases release of ADH from posterior pituitary and aldosterone from adrenal gland


3 main vasoconstrictors

endothelin, AII, and ADH


3 main vasodilators

NO, prostacyclin, ANP

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