Renal response to atrial natriuretic factor is modulated by intrarenal angiotensin II.

The present study in anesthetized dogs (n = 8) was designed to test the hypothesis that intrarenal angiotensin II (ANG II) attenuates the increase in sodium excretion in response to atrial natriuretic factor (ANF). To test this hypothesis, renal hemodynamic and excretory responses to systemically administered ANF (0.3 micrograms.kg-1.min-1) were assessed in the presence of ANG II infusion into the left kidney (ANG II K) at a nonpressor dose (1.5 ng.kg-1.min-1) and with an infusion of saline into the right kidney, the latter which served as control (CK). During ANF infusion, absolute increases in urinary sodium excretion (delta + 160.8 +/- 44.7 vs. delta + 369.4 +/- 56.9 mu eq/min, P less than 0.005) and fractional sodium excretion (delta + 2.55 +/- 0.62 vs. delta + 4.26 +/- 0.82%, P less than 0.03) were markedly attenuated in the ANG II K compared with CK. Glomerular filtration rate increased only in the CK. Urine osmolality decreased in both the ANG II K and CK. These studies demonstrate an attenuated natriuresis to ANF in the presence of intrarenally infused ANG II, which is associated with a blunted increase in glomerular filtration rate. These studies support the hypothesis that the renal hemodynamic and excretory responses to ANF are modulated by intrarenal ANG II.