thromboxane-b2 and Diabetes-Insipidus

A case of familial central diabetes insipidus and dilatation of the urinary tract is reported. Administration of desmopressin for 1 year improved urinary tract dilatation with a concomitant reduction in urine volume. Urinary cyclic adenosine monophosphate and prostaglandin E2 excretion increased after treatment.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Cyclic AMP; Deamino Arginine Vasopressin; Diabetes Insipidus; Dinoprost; Dinoprostone; Humans; Hydronephrosis; Male; Thromboxane B2; Urine

1. The production of prostaglandin (PG) E2, F2 alpha and thromboxane B2 (TXB2) by isolated glomeruli, cortical tubular suspensions and medullary and papillary slices was measured in normal Long-Evans rats 4, 8 and 14 days after starting on oral Na+ load and the results were compared with those of rats on a normal Na+ intake. 2. In glomeruli, PGE2 decreased at days 4 and 8, and returned to normal at 14 days. PGF2 alpha decreased only at day 4 and TXB2 decreased in all Na+-loaded animals. In cortical suspensions, a transient decrease of PGE2 was observed at day 4. In medullary slices, PGE2 and TXB2 decreased in all experimental periods. In contrast, in papillae, a significant increase of PGE2 was observed with Na+ loading at day 8, but PGF2 alpha and TXB2 did not change consistently. 3. Similar changes were observed in rats with hypothalamic diabetes insipidus (DI rats) Na+ loaded for 4 days, as compared with DI rats on a normal Na+ intake. 4. The results suggest that prostanoids participate in the renal adaptation to an increased Na+ intake, and that this response is relatively independent of the presence of antidiuretic hormone.

Topics: Animals; Diabetes Insipidus; Dinoprost; Dinoprostone; Female; Kidney; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats; Sodium; Thromboxane B2; Time Factors; Tissue Distribution

Rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) which are devoid of vasopressin, excrete significantly increased amounts of immunoreactive thromboxane B2 in urine. The increase was corrected by treatment with vasopressin. These results suggest that, in the intact organism, thromboxane synthesis may be under tonic inhibitory control by vasopressin although other renal mechanisms explaining the increase in thromboxane cannot be excluded. Our observations further support an involvement of prostaglandins and thromboxanes in the regulation of water metabolism.

Topics: Animals; Arginine Vasopressin; Diabetes Insipidus; Hypothalamus; Kidney; Male; Rats; Rats, Brattleboro; Thromboxane B2; Thromboxanes; Vasopressins