Abstract
In an attempt to analyze the pathogenesis of hereditary vasopressin-resistant diabetes insipidus (DI) in mice associated with oligosyndactily (Os), possible participation of adenyl cyclase of the kidney cells in the mechanism of diuresis was examined.
In DI Os/+ mice with severe diuresis intraperitoneal injection of adenosine 3', 5'-monophosphate (cyclic AMP) but not exogenous vasopressin delayed the onset of diuretic response to water load, while the reverse was true in DI +/+ mice with mild diuresis. Urinary osmolarity, moreover, was increased by cyclic AMP but not by vasopressin in Os/+ mice, whereas the reverse was the case with +/+ sibs. Although lack or defect of vasopressin-sensitive adenyl cyclase of the kidney cells might be assumed in the severely diuretic mice, both the basal and vasopressin-activated adenyl cyclase activities in vitro were similar between Os/+ and +/+ animals. The defect of vasopressin-sensitive adenyl cyclase in the kidney thus does not seem to be responsible for the hereditary nephrogenic diuresis of mice.
