Overview Introduction The renin-angiotensin-aldosterone system (RAAS) attempts to maintain arterial blood pressure by controlling blood volume a decrease in arterial blood pressure is sensed by the kidneys as decreased renal perfusion pressure this in turn stimulates the juxtaglomerular cells to secrete renin into circulation note that increased sympathetic activity and β1-agonists (e.g., isoproterenol) increase renin secretion renin converts angiotensinogen into angiotensin I, a precursor of angiotensin II angiotensin-converting enzyme (ACE) in the lung and kidneys converts angiotensin I → angiotensin II note that a decrease in Na+ delivery to the macula densa also stimulates RAAS angiotensin II activates type I G protein-coupled angiotensin II receptors (AT1) receptors which acts on the adrenal cortex (zona glomerulosa) to increase aldosterone secretion aldosterone will increase Na+ reabsorption and K+ secretion in the principal cells of the distal tubule and collecting duct aldosterone will also increase H+ secretion in the alpha-intercalated cells directly stimulates the Na+-H+ exchange acts on the hypothalamus to increase thirst and the pituitary to increase anti-diuretic hormone (ADH) secretion ADH will act on the principal cells to increase aquaporin-2 expression this increases the collecting duct's permeability to water and thus increases water reabsorption acts on arterioles to increase total peripheral resistance and thus increasing arterial pressure preferrentially constricts the efferent arteriole to maintain glomerular filtration rate (GFR) in low volume states (e.g., hemorrhaging)