How is RAAS in HTN?

3 stimuli for renin secretion (decreased NaCl in distal henle's loop, decreased pressure or stretch within renal afferent arteriole baroreceptors, sympathetic nervous system stimulation by b1 receptors) Angiotensin type 1 (potent pressor, mitogen stimulates vascular smooth muscles and myocyte growth, role in pathogenesis of atherosclerosis) Angiotensin type 2 (vasodilator, sodium excretion, inhibition of cell growth and matrix, improves vascular remodeling stimulating smooth muscle apoptosis, regulates GFR) AT1 receptor blockade increases AT2 receptor activity. Renin secreting tumors cause renin-dependent HTN, obstruction of renal arteries decrease renal perfusion stimulating renin secretion, excess AT2 contributes to atherosclerosis, cardiac hypertrophy and renal failure and maybe target to prevent organ damage. increased RAAS doesnot mean HTN always, could be physio response/secondary aldosteronism not HTN, seen in edema/CHF/liver.