Natriuresis in Conscious Dogs Caused by Increased Carotid Na+ During Angiotensin II and Aldosterone Blockade

The renal response ot a selective increase in the Na+ concentration of the blood perfusing the central nervous system was investigated in conscious dogs treated wiht the converting enzyme inhibitor enalaprilat and the aldosterone antagonist canrenoate. In split-in- fusion experiments the plasma Na+ of carotid blood was increased (approx. 6nM) by bilateral infusion of hyperonic NaCl. Concomitanly distilled water was infused int the v. cava making the sum of the infusions isotonic. In control experiments isotonic saline was infu- sed at identical rates into all three catheters. Na+ excretion in- creased markedly in both series, 103+/-14 to 678+/-84 mol min-1 during split-infusion and 90+/-14 to 496+/-74 mol min-1 during the isotonic volume expansion. Peak rate of excretion, peak franctional sodium excretion, and cumulative sodium excretion were all signifi- cantly higher (P<0.05) during split-infusion than during control ex- periments. Plasma vasopressin increased only during split-infusion (0.68+/-0.11 to 2.4+/-0.8pg ml-1) while the increases in plasma atrial natriuretic peptide were similar in the two series. Urinary excretion of urodilatin (AnP95-126) increased significantly more during split-infusion (46+/-11 to 152+/-28 fmol min-1) than during the isotonic expansion (45+/-14 to 84+/-16 fmol min-1) (P<0.05). It is concluded that the natriuretic mechanisms activated by a selecti- ve increase in the Na+ concentration of carotid blood and associated withincreased excretion of urodilain cannot be eliminated by block- ade of the renin-angiotensin-aldosterone system