Vasopressin secretion in primary polydipsia and cranial diabetes insipidus.

Vasopressin secretion was studied in a group of 18 patients with polydipsia (urine volume greater than 21/24 h) in whom nephrogenic diabetes insipidus had been excluded. Osmoregulation of vasopressin release was defined by hypertonic saline infusion, and three independent non-osmotic tests of vasopressin release were also applied. A wide spectrum of abnormalities in vasopressin secretion was observed. Four patients seem to have primary polydipsia, since they showed a normal response to osmotic stimulation, but non-osmotic vasopressin release was subnormal in two. The remaining 14 patients had cranial diabetes insipidus, as judged by subnormal or absent vasoprsssin responses to hypertonic saline infusion. Of these 14, five had undetectable vasopressin during osmotic stimulation, but each mounted a response to the non-osmotic stimuli; three of these had familial polyuria. Three further patients appeared to have isolated osmoreceptor defects, showing normal responses to non-osmotic stimuli but none to osmotic stress. Four patients with partial cranial diabetes insipidus, as judged by subnormal vasopressin response to osmotic stimuli, seemed to have normal osmoreceptor function but deficient vasopressin release. There was no correlation between the degree of vasopressin response to osmotic stimuli and the three non-osmotic tests of vasopressin release, and in particular vasopressin release should not replace osmotic tests to define cranial diabetes insipidus.