Atrial natriuretic peptide and the kidney

Abstract

Studies addressing the mechanisms of atrial natriuretic peptide (ANP) action within the kidney are reviewed. The magnitude of the natriuretic response to ANP initially suggested inhibition of renal sodium transport. It now appears, however, that the renal response to ANP is largely dependent on ANP-induced alterations in renal hemodynamics. At the glomerulus, ANP-induced afferent arteriolar dilatation and efferent arteriolar constriction produce a rise in the glomerular capillary hydraulic pressure and thus an increase in the filtration fraction and glomerular filtration rate. Furthermore, angiotensin II-induced increments in renal perfusion pressure markedly augment ANP-induced NaCl excretion, whereas increments in peritubular oncotic pressure or reductions in renal perfusion pressure nearly abolish this natriuretic effect, thereby suggesting that changes in the peritubular physical factors, which govern tubule fluid reabsorption, are required to elicit the natriuretic action of ANP. In addition, increments in papillary vasa recta hydraulic pressures during ANP infusion argue for an important influence of ANP on fluid exchange in the renal papilla. There also is recent evidence to suggest that ANP directly inhibits papillary collecting duct NaCl reabsorption. This action of ANP is thought to contribute to the enhanced renal excretion of sodium-rich urine in response to ANP. Finally, in two models of chronic extracellular volume expansion, namely, mineralocorticoid excess and a reduction in nephron number with a high sodium intake, endogenous plasma ANP levels increased significantly above control levels.(ABSTRACT TRUNCATED AT 250 WORDS)