The role of adrenal steroidogenesis in arterial hypertension.
Adrenal aldosterone production, the major regulator of salt and water retention, is discussed with respect to hypertensive diseases. Physiological aldosterone production is tightly regulated, either stimulated or inhibited, in the adrenal zona glomerulosa by both circulating factors and/or by locally derived endothelial factors. Arterial hypertension caused by volume overload is the leading clinical symptom indicating increased mineralocorticoid hormones. Excessive aldosterone production is seen in adenomatous disease of the adrenals. The balance between stimulatory/proliferative and antagonistic signaling is disturbed by expression of altered receptor subtypes in the adenomas. Increased aldosterone production without a detectable adenoma is the most frequent form of primary aldosteronism. Both increased sensitivity to agonistic signals and activating polymorphisms within the aldosterone synthase gene (CYP11B2) have been associated with excessive aldosterone production. 17alpha-Hydroxylase deficiency and glucocorticoidremediable aldosteronism can also cause excessive mineralocorticoid synthesis. In contrast, the severe form of pregnancy-induced hypertension, preeclampsia, is characterized by a compromised volume expansion in the presence of inappropriately low aldosterone levels. Initial evidence suggests that compromised CYP11B2 is causative, and that administration of NaCl lowered blood pressure in pregnant patients with low aldosterone availability due to a loss of function.
Mohaupt
Markus G
MG
Division of Hypertension, Department of Nephrology/Hypertension, University of Bern, Bern, Switzerland.
D000311:Adrenal Glands / Q000378:metabolism* / Q000502:physiology; D000450:Aldosterone / Q000096:biosynthesis / Q000172:deficiency / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D046110:Hypertension, Pregnancy-Induced / Q000209:etiology; D008901:Mineralocorticoids / Q000096:biosynthesis; D011247:Pregnancy; D013256:Steroids / Q000096:biosynthesis* / Q000502:physiology*
D008901:Mineralocorticoids; D013256:Steroids; D000450:Aldosterone