Involvement of the renal natriuretic peptide urodilatin in body fluid regulation

Urodilatin, a 32-aminoacid peptide, is expressed in distal tubular cells of the human kidney and presumably released into the luminal part of the nephron to exert its effect via activation of membrane-bound guanylyl cyclases (type A) at the medullary collecting duct. Thereby, the tubular reabsorption of sodium is inhibited and natriuresis is stimulated. The peptide is derived from the same gene and propeptide as the atrial natriuretic peptide (ANP), a more N-terminal cleavage in the human kidney than in other body tissues may be responsible for the existence of this renal natriuretic peptide and its increased stability in the extreme environment of the kidney and primary urine. The results of a sequence of human and animal physiology experiments has suggested that the renal natriuretic peptide, rather than its cardiac analog ANP, may play an essential role in mediating urinary sodium excretion. First observations are made suggesting a contribution of the renal natriuretic peptide also to disturbed sodium handling under pathophysiological conditions.