Acute effects of vasopressin on potassium and water balance in rats with diabetes insipidus

In rats with hereditary hypothalamic diabetes insipidus (DI), single injections of vasopressin tannate (50-500 mU/animal) induced a dose dependent potassium retention. Sodium balance was only affected by the highest doses of 250 and 500 mU, which induced sodium retention. Serum potassium concentrations slightly increased or remained unchanged after vasopressin administration, whereas serum sodium concentrations decreased. Serum osmolality did not show a significant decrease. In relation to the dose of vasopressin administered, water intake and urine volume decreased. Concomitantly, water was retained; plasma volume increased and hematocrit decreased. Extrarenal water loss of DI rats, which was elevated when compared with rats heterozygous for DI, was restored toward normal levels under the influence of vasopressin. It is concluded that in DI rats antidiuretic hormone induces potassium retention via a reduction of tubular flow rates in the distal parts of the nephron. Most of the retained potassium is compartmentalized in the intracellular space, whereas most of the retained water remains extracellularly. For DI rats, the substitution dosage of vasopressin tannate should be below the level that induces sodium retention, i.e., about 100 mU/100 g body wt. (39 references).