Renal response to ANP in normal dogs during extreme inhibition of distal Na+ transport

Abstract

Atrial natriuretic peptide (ANP) is thought to exert its major effect within the cortical and inner medullary collecting ducts (CCD and IMCD) by inhibiting Na+ transport along conductive channels and electroneutral pathways. These transport routes are also thought to be inhibited by a combination of amiloride, thiazide and bradykinin. We tested the ability of normal dogs to respond to ANP when various combinations of these Na+ transport inhibitors were present. In 24 dogs ANP raised UNaV from 31 ± 6 to 223 ± 41 μEq/min (P < 0.05), a Δ of 192 μEq/min. Bradykinin alone did not depress ΔUNaV in response to an ANP infusion. In the presence of extreme natriuresis caused by amiloride and thiazide. the response to ANP was magnified, presumably due to augmented Na+ delivery to the CCD and IMCD. When distal delivery of Na+ to one kidney was controlled by aortic clamping in the presence of amiloride, thiazide and bradykinin, ΔUNaV in response to ANP was depressed (48 vs. 168 μEq/min). We conclude that in the presence of extreme inhibition of Na+ transport within the collecting ducts, ANP can still cause a further natriuresis, probably in the absence of augmented distal Na+ delivery.