Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins.

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg ⋅ min-1 ⋅ kg body wt-1), plasma vasopressin concentration increased to 2.30 ± 0.20 pg/ml compared with 0.12 ± 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 ± 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 ± 15.8 μmol/min) than without vasopressin (4.6 ± 0.4 ml/min and 14.4 ± 4.1 μmol/min, respectively). Deamino-[Cys1,d-Arg8]vasopressin, a V2 receptor agonist (4 pg ⋅ min-1 ⋅ kg-1), mimicked the antidiuretic response (0.20 ± 0.03 ml/min) without changing UNaV (9.7 ± 4.4 μmol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 ± 0.02 ml/min), and abolished the natriuresis (13.4 ± 3.7 μmol/min). During AVP infusion, UNaV was highly correlated ( r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.