Corticosteroid-dependent hypertension can be cured by surgical removal of steroid-producing adrenocortical adenomas or, in case of other etiopathologic factors, specific drug therapy may be introduced for preventing irreversible complications of the hypertension process. In most cases, corticosteroid-dependent hypertension fails to manifest itself with clearcut endocrine symptoms. Therefore, an endocrine evaluation is strongly recommended in all patients with hypertension who are susceptible to hypokalaemia and whose blood pressure is poorly controlled with conventional antihypertensive drugs. The increased blood pressure in corticosteroid-producing adrenocortical adenomas may be attributed not only to the main glucocorticoid, cortisol, and the main mineralocorticoid, aldosterone, but also to the actions of weak mineralocorticoids which may be occasionally predominant. Adrenocortical adenomas including incidentalomas produce in different quantities at least 6 corticosteroids which play direct or indirect roles in hypertension. These adenomas are lacking autonomous hormone secretion and they respond to different regulatory impacts (i.e. stress and, by analogy, CRF or ACTH administration) with markedly-increased hormone secretion. Consequently, hypertension and hypokalaemia develop, often in the absence of other endocrine symptoms. The weak mineralocorticoids may not entirely account for the hypertension, although they may be useful indicators or may serve as precursors for the generation of more potent hypertensinogen steroids and steroid metabolites. This is patently indicated by the disappearance of hypertension, hypokalemia and mineralocorticoid-excess induced suppression of the renin-angiotensin system after the surgical removal of adrenocortical adenomas which produce only weakly-hypertensinogen corticosteroids.
|Pages (from-to)||1139-1144, 1147|
|Publication status||Published - May 28 1989|
ASJC Scopus subject areas