Hormonally maintained high blood pressure following adrenalectomy in rats with adrenal-regeneration hypertension and its possible significance in the etiology of that disorder.

Abstract

Rats were caused to develop adrenal-regeneration hypertension, and attempts were made to reproduce in them after adrenalectomy the same rate of blood pressure rise as occurred in animals allowed to retain enucleated adrenals, by using aldosterone, corticosterone, or a mixture of the two. Corticosterone at 2.5 mg/day caused a somewhat greater rate of blood pressure increase than occurred in rats retaining regenerating glands, but whereas the latter did not manifest thymus involution, hormone-treated animals did. At 1 mg/day there was a drop in blood pressure following adrenalectomy in rats with adrenal-regeneration hypertension, although not always to normotensive levels, and the characteristic hypotension of adrenalectomized rats was prevented. Rats given 100 μg/day of aldosterone following adrenalectomy maintained a continued rise of blood pressure, the rate not differing significantly from that seen in rats with continuing adrenal-regeneration hypertension. Such rats did not display thymus involution, and the blood pressure response was no greater when 1 mg/day of corticosterone was added to the regimen. It is concluded that if the profile of hypertension and failure to cause thymus involution are valid criteria for establishing the identity of the hormone(s) which cause adrenal-regeneration hypertension, aldosterone appears to qualify. Some reasons for doubting the reliability of these criteria and some of the difficulties encountered in attempting to compare quantitatively the effects of endogenously secreted hormone with exogenously administered hormone are given.