EXAGGERATED BLOOD-PRESSURE RESPONSE TO ANGIOTENSIN-II IN PATIENTS WITH CUSHINGS-SYNDROME DUE TO ADRENOCORTICAL ADENOMA

We studied the roles played by the renin-angiotensin system in inducin g hypertension in nine patients with Gushing's syndrome (CS) resulting from adrenocortical adenoma, and compared them with those in patients with primary aldosteronism (PA), renovascular hypertension (RVH) and essential hypertension (EH). In the CS group, each parameter, includin g serum potassium, plasma renin activity, plasma aldosterone, deoxycor ticosterone and corticosterone concentrations, is within the normal ra nge. However, plasma renin activity in the CS group was lower than tha t in the RVH group but higher than that in the PA group, and plasma al dosterone concentration was lower than that in each RVH or PA group. T hese findings indicated that the CS group had a different type of hype rtension from that in either RVH or PA, in which the renin angiotensin system or mineralocorticoids play an important role in hypertension. Meanwhile, captopril (50 mg) administration either with or without ind omethacin pretreatment decreased the mean blood pressure in the CS gro up, although captopril failed to change it in the PA group or in norma l subjects. Furthermore, the presser response to exogenous angiotensin II in the CS group was higher than that in the RVH or EH group, but w as not different from that in the PA group. Thus, the hypertension in patients with CS due to adrenocortical adenoma appears to be mediated through a change in the renin-angiotensin system in the form of exagge rated presser responses to angiotensin II.