Peripheral metabolism of corticosteroids as a mechanism of potency modulation

in Journal of Endocrinology
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In some fields of steroid endocrinology, it has long been accepted that the potency of a hormone may depend not only on its secretion rate and rate of hepatic clearance but also on specific metabolic transformation at the site of the target cell. The crucial role of tissue 5α reductase activity on the action of testosterone is a spectacular example (Peterson, ImperatoMcGinley, Gautier & Sturla, 1977). Curiously—it is easy to be wise after the event—this line of thought seems rarely to have been exercized in explanations of corticosteroid action. Clearly, the severity of diseases of corticosteroid excess, of which Cushing's and Conn's syndromes are the best known examples, is strongly correlated with the secretion rate of cortisol and aldosterone respectively. However, in some forms of hypertension where deranged corticosteroid action might be expected to provide an acceptable explanation (e.g. increased mineralocorticoid secretion in low-renin essential hypertension), no abnormalities of secretion


      Society for Endocrinology

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