The renin-angiotensin-aldosterone system (RAAS) is one of the most important neurohormonal systems that regulate arterial blood pressure and sodium and fluid content in the body In response to decreased sodium, fluid volume, or arterial blood pressure, renin is released from the kidneys converting angiotensinogen to angiotensin I Subsequently, angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II Angiotensin II then increases aldosterone secretion from the adrenal cortex leading to increased sodium and fluid retention in the collecting tubules of the kidneys Angiotensin II is also a potent vasoconstrictor that ultimately increases systemic vascular resistance and arterial pressure
Angiotensin II itself is involved in two negative feedback mechanisms that help regulate the RAAS In short loop negative feedback, elevated angiotensin II stimulates the angiotensin receptors on juxtaglomerular cells to inhibit renin release In long loop negative feedback, elevated blood pressure and sodium levels secondary to angiotensin II eventually decrease renin release via intrarenal baroreceptor and maculadensa pathways, respectively

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