Ramirez G, Ganguly A, Brueggemeyer C D
Department of Internal Medicine, James A. Haley Veterans Administration Hospital, Tampa, Florida 33612.
J Clin Endocrinol Metab. 1988 Jan;66(1):46-50. doi: 10.1210/jcem-66-1-46.
The aldosterone secretory response to Captopril (12.5 mg, orally) was studied in five normal men. Endogenous ACTH and epinephrine secretion was stimulated by the induction of hypoglycemia. Normally this stimulus increases plasma cortisol, GH, aldosterone, and PRA. Administration of captopril resulted in a blunted plasma aldosterone response to hypoglycemia, but no concomitant blunting of the plasma cortisol response. The responses of other hormones, with the exception of PRA, were not affected. When exogenous ACTH was administered to the same men with and without captopril, the plasma aldosterone response was again blunted by captopril, while the plasma cortisol response was unaffected. We conclude that angiotensin II may be required for ACTH to stimulate aldosterone secretion. Alternatively, the possibility that captopril may selectively inhibit aldosterone secretion at the adrenal cellular level cannot be excluded.
对五名正常男性研究了卡托普利（12.5毫克，口服）对醛固酮分泌的反应。通过诱导低血糖刺激内源性促肾上腺皮质激素（ACTH）和肾上腺素分泌。正常情况下，这种刺激会增加血浆皮质醇、生长激素（GH）、醛固酮和肾素活性（PRA）。给予卡托普利导致血浆醛固酮对低血糖的反应减弱，但血浆皮质醇反应未同时减弱。除PRA外，其他激素的反应未受影响。在相同男性中，无论有无卡托普利，给予外源性ACTH时，卡托普利再次使血浆醛固酮反应减弱，而血浆皮质醇反应未受影响。我们得出结论，ACTH刺激醛固酮分泌可能需要血管紧张素II。或者，不能排除卡托普利可能在肾上腺细胞水平选择性抑制醛固酮分泌的可能性。
