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.