Steroid hormones and hypertension: The cortisol-cortisone shuttle
1993; Elsevier BV; Volume: 58; Issue: 12 Linguagem: Inglês
10.1016/0039-128x(93)90104-u
ISSN1878-5867
AutoresPaul M. Stewart, Christopher B. Whorwood, Brian R. Walker,
Tópico(s)Pharmacological Effects of Natural Compounds
ResumoThe role of adrenal steroid hormones in hypertension has, until recently, focused on disorders of secretion. We describe a new form of mineralocorticoid hypertension which arises from impaired metabolism of physiological glucocorticoid. 11 β-hydroxysteroid dehydrogenase (11 β-HSD) is responsible for the inactivation of cortisol to cortisone. Congenital absence of this enzyme (the syndrome of apparent mineralocorticoid excess) results in cortisol acting as a potent mineralocorticoid. Furthermore, inhibition of this enzyme by glycyrrhizic and glycyrrhetinic acids also accounts for the mineralocorticoid excess states seen following licorice and carbenoxolone ingestion. Whilst impaired 11 β-HSD activity has been shown in patients with "essential" hypertension, the significance of this finding remains unknown. These clinical studies, however, have uncovered a novel physiological mechanism, whereby the mineralocorticoid receptor (which in vitro has an equal affinity for cortisol and aldosterone) is protected from cortisol excess by the action of 11 β-HSD. Thus 11 β-HSD plays a crucial role in determining the in vivo specificity for this receptor. (Steroids 58:614–620, 1993)
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