The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.
Part of the book: Renin-Angiotensin Aldosterone System