Atrial natriuretic factor does not inhibit basal or angiotensin II-stimulated proximal transport.

Atrial natriuretic factor (ANF) can functionally overcome the effects of angiotensin II in several tissues. Since ANF and angiotensin II in physiological concentrations have opposite effects on renal sodium excretion, we evaluated whether functional antagonism of the two hormones occurs in the proximal convoluted tubule, as has been recently reported with use of the shrinking split-droplet technique. We used the more conventional technique of in vivo microperfusion to measure the response to systemic ANF (0.5 micrograms.kg-1.min-1) when the endogenous angiotensin II level and proximal transport were normal or when transport was first stimulated by systemic angiotensin II administration (20 ng.kg-1.min-1). In both cases, ANF did not significantly alter bicarbonate, chloride, or water transport in either the early or late proximal convoluted tubule. This inability by ANF to directly affect proximal transport is consonant with the known lack of high-affinity receptors and appropriate second messenger system for ANF in the proximal convoluted tubule.