ABSTRACT
The authors have studied on 50 patients hospitalized in the Adrenal Pathology unit of the Institute of Endocrinology, the etiopathogeny of arterial hypertension (AH) in hypercorticism and the therapeutic implications, arriving at the conclusion that in 20% of the cases AH was probably due to an increased activity of renin-angiotensin and in 47% to elevated levels of aldosterone. The authors hypothesize that AH in the remaining 30% of the hypercorticism cases in this study is due to other mineralocorticoids in excess and suggest that the treatment should be pathogenic and strictly individualized.
Subject(s)
Adrenocortical Hyperfunction/complications , Aldosterone/blood , Hypertension/etiology , Renin/blood , Adult , Electrolytes/blood , Female , Humans , Male , Middle Aged , Mineralocorticoids/bloodABSTRACT
The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.
