MECHANISM OF VASOPRESSIN NATRIURESIS IN THE DOG - ROLE OF VASOPRESSINRECEPTORS AND PROSTAGLANDINS

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). Duri ng infusion of vasopressin (50 pg.min(-1).kg body wt(-1)), plasma vaso pressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0 .12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin i nfusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 mu mo l/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 m u mol/min, respectively). Deamino-[Cys(1),D-Arg(8)]vasopressin, a V-2 receptor agonist (4 pg.min(-1).kg(-1)), mimicked the antidiuretic resp onse (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 mu mol/ min). Indomethacin given during arginine vasopressin (AVP) infusion su ppressed prostaglandin E-2 excretion, intensified the antidiuresis (0. 10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 mu mo l/min). During AVP infusion, UNaV was highly correlated (r = 0.85) wit h prostaglandin Ea excretion. Blood pressure, glomerular filtration ra te, plasma atrial natriuretic peptide concentration, and the rate of p roximal tubule reabsorption (derived from lithium clearance) were simi lar in all series. The data indicate that, in the dog, physiological a mounts of vasopressin can induce natriuresis, probably through activat ion of non-V-2 receptors and the intrarenal synthesis of prostaglandin s.