Renal natriuretic peptide (urodilatin?) and atriopeptin: evolving concepts.

The discovery of the natriuretic peptide, urodilatin, in human urine, together with data from renal cell cultures, immunocytochemistry, radioimmunoassays, and other techniques, strongly indicates that distal tubules in the kidney produce a natriuretic prohormone that may be identical to the 126-residue prohormone of atrial natriuretic peptide [proANP-(1-126)] produced by cardiac atria. The 32-residue peptide, urodilatin [ANP-(95-126)], is found in urine but not in plasma; its natriuretic potency equals or exceeds that of atriopeptin [ANP-(99-126)]. It is still unclear whether urodilatin is the only, or even the primary, renal natriuretic peptide. Circumstantial evidence suggests that natriuretic peptide produced in connecting and collecting tubules may be a principal physiological ligand for more distal "ANP" receptors, but this issue is far from settled. Evidence that the kidneys produce their own natriuretic peptide may partly explain why investigations of the effects of endogenous atriopeptin on renal sodium excretion often have yielded inconsistent results. This inconsistency has led to a gradual evolution of opinion concerning the functional role of atriopeptin. Based on current data, it is postulated that atriopeptin is primarily a regulator of the cardiovascular system and that renal natriuretic peptide participates in the intrarenal regulation of sodium and chloride transport.