Arginine vasopressin potentiates natriuretic effect of atrial peptide

We investigated potentiation of atrial peptide (AP)-induced natriuresis by vasopressin in anesthetized rats. Increasing doses of vasopressin potentiated AP-induced natriuresis in a dose-dependent manner, e.g., sodium excretion during AP administration (290 ng/min) was 0.66 +/- 0.16, 2.02 +/- 0.68, 5.21 +/- 1.38 and 7.08 +/- 1.96 mu eq/min during infusion of 0.00, 0.78, 1.56, and 3.12 ng.kg-1.min-1 of vasopressin, respectively. Vasopressin alone had no effect on sodium excretion. In a second experiment, vasopressin (1.56 ng.kg-1.min-1) potentiated AP (128 ng/min)-induced natriuresis similar to that seen in the first experiment. In this experiment, glomerular filtration rate (GFR) and mean arterial pressure were monitored. Mean arterial pressure was no different between the groups treated with AP plus vasopressin and AP alone. Glomerular filtration was actually reduced in the group treated with vasopressin plus AP, suggesting that neither changes in GFR nor blood pressure were responsible for potentiation of the natriuresis. A third experiment compared the ability of 1-desamino-8-D-arginine vasopressin (dDAVP), a nonpressor analogue of vasopressin, to vasopressin in enhancing AP (145 ng/min)-induced natriuresis. The nonpressor analogue did not potentiate AP-induced natriuresis, whereas vasopressin had the same effect as in the first two experiments. These are the first studies to report a functional interaction between AP and vasopressin. They show that vasopressin potentiates AP-induced natriuresis without altering mean arterial pressure or GFR.