lecture 19 Flashcards
how is covid19 related to the angiotensin 2 disease state
SARSCoV2 spike proteins bind to target cells via angiotensin converting enz 2 > inhibition of ACE2 + decreased ACE2 expression in infected cells > higher circulating levels of Ang2
what are the harmful effects of ang2 and how does body stop it
ang2 can cause damage to tissues
- in alveoli = decrease lung uptake oxygen
- in cardiac myoc = CHF
can also cause inflammation and apoptosis
stop by ACE2 break down to ang1-7 and can bind to MAS1 R to counteract harmful effects
how does BV correlate with BP
= increase BV = increase pressure on walls of blood vessels
= increase BV > increase venous return to heart > increased stroke volume > increased cardiac output > increased BP
how does increased SNS input to kidney act contribute to hypertension
increase SNS input to kidneys > increase renin > increase ang2 = decreased renal Na secretion = BV increases BP increases (these effects can contribute to chronic hypertension)
what is renal SNS involvement in hypertension
efferent renal sns act. usually increases hypertension
- (chronic lowlevel renal nerve stim induces hypertension)
- sympatholytic drugs decrease BP
how can the renin-angio system be manipulated to clinically decrease BP
inhibition via
AT1 anta
ACE inhibi
b blockers
whats AT1 R anta clinically useful for + ex
useful for lowering BP
- Cozaar = angiotensin 2 R blocker (ARB)
- decrease vasocon
- decreases release of aldosterone
whats ACE inhibitors clinically useful for + ex
useful for lowering BP
- inhibits ACE > deccrease amount of angiotensin 2 produced = lower BP
whats b blocker clinically useful for + ex
lowering BP
- decrease ang2 production
- inhibit renin release from JG cells caused by SNS act
- b blocker decrease BP by inhibiting the blood pressure increasing effects of ang2 (vasocon + incr salt intake + increase water in)
What is CHF
heart failture due to reduction of contractility of heart > decrease stroke volume > decrease BP > this decrease cardiac output causes activation of compensatory system (Vasopressin RAS SNS) and to increase fluid retention to increase volume of blood delivered to heart
- increase volume stretches muscles (result in decreasing SV and fluid accumulation in tissues)
describe starling’s law
drop in BP causes increase fluid retention > increased volume of blood increases stroke volume
The greater that the heart muscle is stretched during diastole the greater the force of contraction during systole
CHF in the right side of the heart
- failure of right ventricle = accumulation of blood in right heart + venous system >blood vessels accum in capillaries = weaker + fluid build up in tissue > edema (more pronounced in lower extremities due to grav)
CHF in the left side of the heart
- failure of left side = accumulation of blood in pulmonary circulation > blood in lungs = cant breath
treatments for CHF?
AT1 anta - decrease effects of ang2 > decrease retention of Na and water and decrease vasocon
ACE inhib - decrease production of ang2
b blockers - decrease SNS mediated production of ang2
diuretics - increase excretion of na and water by kidneys (loop stronger than thiazide)
describe function of loops of henle, thick ascending limb, distal con tubule
loop of henle = sire for water reabsorption driven by hyperosmotic interstitium of renal medulla
thick ascending limb = site of Na K Cl reuptake transport
distal convoluting tub = site of na reuptake trans