Diuretic response to acute hypoxia in the conscious dog.

Experiments were performed to determine the renal effects of acute hypoxia in conscious normovolemic dogs. Dogs were made hypoxic and also became hypocapnic through increased ventilation. Hypocapnic hypoxia was associated with increased urine flow, arterial blood pressure, cardiac output, PAH and inulin clearance, and electrolyte excretion. Urinary excretion of prostaglandin E2 (PGE2) also increased during hypocapnic hypoxia. To test whether the respiratory alkalosis accompanying hypoxic exposure was important in mediating the observed response, experiments were conducted in which the dogs were hypoxic but remained isocapnic via addition of CO2 to the inspired gas. Urine flow increased and was associated with changes in renal function and hemodynamics similar to those during hypocapnic hypoxia. Experiments were also conducted to determine whether the increased PGE2 release in hypoxia was functionally significant. Dogs were pretreated with meclofenamate and then made hypoxic. Prostaglandin synthesis inhibition did not alter the renal response to hypocapnic hypoxia. Dogs were also treated chronically with propranolol in an attempt to blunt the rise in blood pressure during hypoxia. In dogs with only a small transient increase in blood pressure, the diuresis was blocked. It is concluded that systemic hypoxia results in a mild diuresis in the conscious normovolemic dog. This response occurs independent of changes in arterial pH or renal prostaglandin release. The diuretic effect of hypoxia is probably due to increased renal perfusion pressure and resultant increased filtration.