Diuretic response to acute hypoxia in the conscious dog

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Abstract
Experiments were performed to determine the renal effects of acute hypoxia in conscious normovolemic dogs. Dogs were made hypoxic and became hypocapnic through increased ventilation. Hypocapnic hypoxia was associated with increased urine flow, arterial blood pressure, cardiac output, PAH [p-aminohippurate] 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 also determined whether the increased PGE2 release in hypoxia was functionally significant. Dogs were pretreated with meclofenamate and then made hypoxic. PG synthesis inhibition did not alter the renal response to hypocapnic hypoxa. Dogs were 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 during hypoxia. In dogs with only a small transient increase in blood pressure, the diuresis was blocked. Apparently, systemic hypoxia results in a mild diuresis in the conscious normvolemic dog. This response occurs independent of changes in arterial pH or renal PG release. The diuretic effect of hypoxia is probably due to increased renal perfusion pressure and resultant increased filtration.

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