Abstract

This chapter discusses the regulation of the formation of glucocorticoids and mineralocorticoids in vivo. Recent findings clearly demonstrate a different regulation for the biosynthesis of glucocorticoids and mineralocorticoids. The renin–angiotensin system is the main regulator of aldosterone synthesis. Recent findings have also clearly established that a low sodium or high potassium intake are factors that control the expression of the early and final steps of mineralocorticoid formation. It is suggested that adrenocorticotropin (ACTH) is the principal factor involved in the control of glucocorticoid biosynthesis and secretion, whereas many other factors participate in mineralocorticoid metabolism. ACTH binds to specific cell membrane receptors and induces the formation of cyclic adenosine monophosphate (cAMP) and the activation of protein kinase A. At short term, ACTH activates the transport and the availability of cholesterol to mitochondrial P450scc to facilitate the formation of pregnenolone. The synthesis of new P450scc protein does not appear necessary, at least for the short term effect of ACTH. It is suggested that a predominant role is played by P45017α in the control of glucocorticoid synthesis.

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