Role of intrarenal ANG II in reflex neural stimulation of plasma renin activity and renal sodium reabsorption

Renal sympathetic stimulation of plasma renin activity (PRA) and sodium reabsorption was examined in conscious dogs before and during intrarenal angiotensin II (ANG II)-type 1 receptor blockade with losartan (Dup-753) and converting enzyme inhibition. In uninephrectomized dogs, renal function and PRA responses to 14% blood volume depletion (BVD) were measured. BVD was utilized to activate renal sympathetic outflow in the absence of hypotension. In eight vehicle-treated dogs, 14% BVD increased PRA from 1.38 ± 0.32 to 2.79 ± 0.66 ng ANG I · ml^-1 · h^-1 and decreased urinary sodium excretion (U(Na)V) from 85.1 ± 11.3 to 45.4 ± 7.5 μeq/min. During losartan (n = 6) and captopril (n = 5) infusion, plasma renin responses were enhanced in response to 14% BVD (1.93 ± 0.48 to 5.74 ± 2.25 and 3.03 ± 0.73 to 9.19 ± 1.94 ng ANG I · ml^-1 · h^-1, respectively), whereas antinatriuretic responses were similar to vehicle-infused dogs. Thus, neurogenic antinatriuresis is not mediated by secondary generation of ANG II, since U(Na)V decreased similarly to control in all conditions of ANG II blockade. Tonic intrarenal and/or circulating ANG II synthesis of dogs on a normal sodium diet inhibit neurogenic stimulation of renin release, since PRA responses were enhanced after blockade of ANG II.