POSTPRANDIAL NATRIURESIS IN HUMANS - FURTHER EVIDENCE THAT URODILATIN, NOT ANP, MODULATES SODIUM-EXCRETION

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mu mol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary e xcretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/ min. The effect of high-salt intake on urinary sodium, chloride, and u rodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin an d sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which wa s acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriu retic profile, and no positive correlation between plasma ANP and sodi um excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily i nvolved in the regulation of the excretion of sodium and chloride.