ABSTRACT
Physiologic Actions of ANP Renal actions of ANP include increasing the glomerular filtration rate (GFR) and, therefore, the filtered load of Na+. It does this by vasodilating afferent arterioles, vasoconstricting efferent arterioles, and possibly increasing glomerular membrane permeability. Receptors for ANP are found on glomerular mesangial cells, where ANP-stimulated relaxation presumably increases the effective surface area for filtration. Atrial natriuretic peptide also decreases renin secretion by juxtaglomerular (JG) cells of afferent arterioles, which has the indirect effects of decreasing plasma angiotensin II and III concentrations, reducing peripheral resistance, and decreasing aldosterone secretion. Inhibition of NaCI reabsorption by the collecting ducts also occurs due to the presence of ANP. Although this effect may be augmented by reduced aldosterone levels, ANP has been found to act directly on cells of medullary collecting ducts through its second messenger, cyclic guanosine monophosphate (cGMP). Through cGMP, ANP apparently inhibits Na+ channels from opening in apical membranes, thereby reducing NaCI reabsorption. Atrial natriuretic peptide also reduces the ability of ADH to act on medullary collecting ducts. Through these combined influences on renal function, ANP causes natriuresis and diuresis.
