Role of vasopressin in the impaired water excretion of glucocorticoid deficiency

Abstract

The mechanism whereby glucocorticoid deficiency impairs renal water excretion was studied in the conscious mineralocorticoid-replaced, adrenalectomized rat. Control animals received physiologic replacement with prednisolone, and experimental animals were deprived of glucocorticoid hormone for either 1 or 14 days. The control animals excreted 95 +/- 1.9% of an acute water load (30 ml/kg) in 3 hours, a value significantly higher than the volume excreted by animals deprived fo glucocorticoid hormone for 1 day (70.0 +/- 3.6%, P less than 0.01) and 14 days (40.0 +/- 3.9%, P less than 0.01). Following the acute water load, plasma vasopressin levels, as measured by radioimmunoassay, was 1.08 pg/ml in the control rats, a value significantly lower than values obtained after the water load in rats deprived of glucocorticoid hormone for 1 day (2.5 +/- 0.2 pg/ml, P less than 0.01) and 14 days (2.4 +/- 0.3 pg/ml, P less than 0.01). To further examine the effect of plasma vasopressin in the impaired water excretion of glucocorticoid deficiency, we performed studied in Brattleboro rats with central diabetes insipidus. In these animals with absence of vasopressin, a defect in water excretion was observed after 14 days, but no 1 day, of glucocorticoid deficiency. In Sprague-Dawley rats, the impaired water excretion after 14 days of glucocorticoid deficiency was associated with a significantly lower cardiac index (209 +/- 14 vs. 291 +/- 11 ml/min/kg, P less than 0.01) and renal blood flow (3.8 +/- 0.3 vs. 5.7 +/- 0.2 ml/min/g, P less than 0.01) than that observed after 1 day of glucocorticoid deficiency. In diabetes insipidus rats, after 14 days of glucocorticoid deficiency, the percentage of an acute water load excreted (121 +/- 7% vs. 158.7 +/- 7.0%, P less than 0.01) was lower than that observed after 1 day of glucocorticoid deficiency. In summary, the present results indicate that glucocorticoid deficiency impairs renal water excretion by both vasopressin-dependent and vasopressin-independent mechanisms. The vasopressin-dependent renal mechanism is associated with a marked decrease in both systemic and renal hemodynamics.