Abstract
Familial hypothalamic diabetes insipidus ( DI) has arisen as an apparently spontaneous mutation from a strain of Long-Evans hooded rats being bred for unrelated researches not involving radioactivity. The DI rats decrease water intake and urine flow, and increase urine osmolality in response to injected vasopressin. They concentrate their urines only minimally or not at all in response to dehydration, hypertonic saline, nicotine, or stress, and their serum osmolalities and sodium concentrations are significantly higher than those of normal animals. They show marked diminution of neurosecretory material in the neurohypophysis and supraoptic nucleus. The data suggest that the deficiency causing DI in these rats is a lack or dearth of synthesis of vasopressin or its carrier protein, or both.
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