Figure 20-19 Interactions between atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone system. Hypotension or hypovolemia triggers the release of renin from the afferent arteriole, thereby causing the formation of angiotensin II, which stimulates the release of aldosterone from the adrenal cortex. Angiotensin II and aldosterone cause vasoconstriction and sodium retention, ultimately resulting in re-expansion of intravascular volume; this volume re-expansion causes atrial distention, which triggers the release of ANP. ANP inhibits the release of renin, renin's action on angiotensinogen to form angiotensin II, angiotensin-induced vasoconstriction, stimulation of aldosterone secretion by angiotensin II, and the action of aldosterone on the collecting duct. Thus, the actions of ANP promote vasodilation and sodium excretion. Therapeutic administration of fluids to distend the atrium and release ANP is an important intervention to curtail renal vasoconstriction and sodium retention.