Abstract
Experimental hyperadiuretism in pregnant rats was induced by applying them daily throughout the pregnancy a synthetic analogue of vasopressin--dDAVP (1-deamino-8-D-arginine vasopressin). It brought about a moderate alteration in the ability to produce hypertonic urine in their offsprings. The osmoregulatory function in the offsprings in the course of fetal development could have been suppressed either by a direct or an indirect effect of dDAVP i.e. by the hypotonicity of mothers' internal environment. There is by now some evidence based on the simultaneous determination of urinary vasopressin and osmolality that the impairment of the osmoregulatory function may be, at least partly, on the renal level.
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