RAAS intro Flashcards
reducing factors of EABV
less blood volume, increased capacitance, reduced cardiac output
4 baroreceptors
aortic arch, LV, carotid sinus, juxtaglomerular apparatus
renin fn
cleaves angiotensinogen to angiotensin I, initiating RAAS cascade
renin source
renal juxtaglomerular apparatus, modified SMCs located in the media of afferent arteriole
what stimulates renin release
decreased circulating volume- leads to baroreceptor signals and greater sympathetic tone, also less Cl- in macula densa tubule
source of angiotensinogen
liver
ACE fn
convert angiotensin I to angiotensin II by cleaving C terminal peptide, also breaking down endogenous bradykinin
fn of AII
direct effect on arteriole vasoconstriction, stimulates aldosterone release from adrenal gland as well (Na and water retention, higher volume and BP)
origin of ACE inhibitors
isolated from brazilian pit viper venom
regulation of RAAS?
primarily feedback loops, causes of less renin release: high AII, less sympathetic activity, less reabsorption of Na (higher ECF and systemic pressure), higher renal perfusion pressure
main takeaway: the effects of AII eventually inhibit renin secretion
list steps from lower circulating volume to increased sympathetic tone
lower volume - lower venous return - lower CO (less preload) - lower BP - baroreceptor response - higher sympathetic tone
immediate effects of elevated SNS related RAAS
Venous constriction, high contractility, arteriole constriction, renin secretion (AII forms and more vasoconstriction), tubular Na reabsorption
when are ACE inhibitors less effective
low renin hypertension- better for CCB and diuretics
most ppl w/ EH have high-renin hypertension
renin and aldo status in 3 renal causes of secondary HT
CKD= high renin and aldo
renal artery stenosis= high renin and aldo
primary aldosteronism= low renin and high aldo (primary high aldo inhibits renin secretion)
RAAS response to CHF
perceives low volume, activates RAAS to increase Na retention and venous pressure- causes edema
