Interactions between angiotensin II and renal nerves during chronic sodium deprivation.

The aim of this study was to examine the importance of the renal nerves in mediating the sodium-retaining actions of angiotensin II (ANG II) during chronic sodium deprivation. In seven female dogs the left kidney was denervated and the urinary bladder was split, allowing continuous urine collection from separate innervated and denervated kidneys in the same dog. The dogs were maintained on a low-sodium diet (7 meq/day) for 9 days and then infused with the converting-enzyme inhibitor captopril (CAP, 14 micrograms.kg-1.min-1, 7 days) followed by CAP plus ANG II (10 ng.kg-1.min-1, 7 days). Mean arterial pressure (MAP) fell from a control of 88 +/- 4 (average for 5 days preceding CAP) to 65 +/- 3 mmHg during CAP. Infusion of ANG II along with CAP restored MAP to 97 +/- 5 mmHg. There were no significant differences in urine volume or sodium, potassium, chloride, or osmolar excretions between innervated and denervated kidneys during the control period, CAP infusion, or CAP plus ANG II infusion. Norepinephrine content was reduced by 99 +/- 1% in denervated kidneys. Because a differential response was not observed between innervated and denervated kidneys during ANG II blockade or infusion of ANG II, we conclude that the renal nerves do not play a major role in mediating the sodium-retaining effects of ANG II during chronic sodium restriction.