NATRIURESIS IN CONSCIOUS DOGS CAUSED BY INCREASED CAROTID [NA-II AND ALDOSTERONE BLOCKADE(] DURING ANGIOTENSIN)

The renal response to a selective increase in the Na+ concentration of the blood perfusing the central nervous system was investigated in co nscious dogs treated with the converting enzyme inhibitor enalaprilat and the aldosterone antagonist canrenoate. In split-infusion experimen ts the plasma [Na+] of carotid blood was increased (approx. 6 mM) by b ilateral infusion of hypertonic NaCl. Concomitantly distilled water wa s infused into the v. cava making the sum of the infusions isotonic. I n control experiments isotonic saline was infused at identical rates i nto all three catheters. Na+ excretion increased markedly in both seri es, 103 +/- 14 to 678 +/- 84 mu mol min(-1) during split-infusion and 90 +/- 14 to 496 +/- 74 mu mol min(-1) during the isotonic volume expa nsion. Peak rate of excretion, peak fractional sodium excretion, and c umulative sodium excretion were all significantly higher (P < 0.05) du ring split-infusion than during control experiments. Plasma vasopressi n increased only during split-infusion (0.68 +/- 0.11 to 2.4 +/- 0.8 p g ml(-1)) while the increases in plasma atrial natriuretic peptide wer e similar in the two series. Urinary excretion of urodilatin (ANP95-12 6) increased significantly more during split-infusion (46 +/- 11 to 15 2 +/- 28 fmol min(-1)) than during the isotonic volume expansion (45 /- 14 to 84 +/- 16 fmol min(-1)) (P < 0.05). It is concluded that the natriuretic mechanisms activated by a selective increase in the Naf co ncentration of carotid blood and associated with increased excretion o f urodilatin cannot be eliminated by blockade of the renin-angiotensin -aldosterone system.