Atrial natriuretic peptide has no direct effect on proximal tubule sodium and water reabsorption.

Infusion of ANP has been shown to increase the urinary excretion of sodium and water. However it is still controversial in which tubular segment sodium reabsorption is inhibited. To clarify this problem we have performed in vivo and in vitro studies to examine the direct effect of ANP on rat proximal tubules. The in vivo effect of ANP has been tested by using the micropuncture technique and in particular the shrinking droplet method that allows each investigated tubule to serve as its own control. Addition of either low (10(-9) M) or high (2 x 10(-6) M) concentrations of ANP to the luminal perfusate resulted in no significant change in isotonic fluid reabsorption (Jv). The same holds when the proximal tubules were perfused on both the tubular and peritubular side, with modified Ringer solution containing 10(-9) M ANP. To examine possible in vitro effects of ANP we prepared highly purified proximal tubule suspension derived from rat renal cortex and monitored oxygen consumption (QO2) that is tightly coupled to sodium transport in this segment. Synthetic ANP, either at low (10(-9) M) or at high (10(-6) M) concentrations, did not affect basal rate of tubular respiration. Moreover the peptide hormone (10(-9) M) did not inhibit nystatin stimulated and ouabain sensitive QO2. These results indicate that the enhancement of renal sodium excretion induced by ANP is not related to a direct inhibition of sodium transport in the proximal tubule.