Figure 1: Schematic drawing of the circulating renin-angiotensin-aldosterone system (RAAS). RAAS is controlled at the level of renin. The reduced intra-luminal pressure in the afferent arteriole (renal hypoperfusion), reduced sodium concentration in the distal tubular fluid, and increased local sympathetic nerve activity stimulate renin release from Juxtaglomerular cells; in bloodstream, renin converts angiotensinogen to angiotensin I; angiotensin converting enzyme (ACE), rich in pulmonary vasculature, further converts angiotensin I to angiotensin II; angiotensin II stimulates adrenal gland at zona glomerulosa to secrete aldosterone; and lastly, aldosterone acts on kidney tubules to increase absorption of Na+ and excretion of K+. Na+ absorption leads to intravascular volume expansion.