Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs.

The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +/- 5.1 vs. 103.0 +/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +/- 20.1 vs. 86.3 +/- 15.1 mumol Na+/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +/- 16.8 vs. 128.3 +/- 32.2 mumol Na+/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II.