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Aldosterone synthase, also called steroid 18-hydroxylase, corticosterone 18-monooxygenase or P450C18, is a steroid hydroxylase cytochrome P450 enzyme involved in the biosynthesis of the mineralocorticoid aldosterone and other steroids. The enzyme catalyzes sequential hydroxylations of the steroid angular methyl group at C18 after initial 11β ...
The genes encoding aldosterone synthase and 11β-hydroxylase are 95% identical and are close together on chromosome 8. In individuals with GRA, there is unequal crossing over so that the 5' regulatory region of the 11-hydroxylase gene is fused to the coding region of the aldosterone synthase. [citation needed]
Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex; 11β-hydroxylase is found in the zona glomerulosa and zona fasciculata. Steroidogenesis, showing aldosterone synthesis at upper-right corner. [13] Aldosterone synthase is normally absent in other sections of the adrenal gland. [14]
18-Hydroxylase (aldosterone synthase) – mineralocorticoid synthesis 21-Hydroxylase – corticosteroid synthesis Cytochrome P450 ( CYP1 , 2 , 3 ) – estrogen metabolism
Lorundrostat (developmental name MLS 101) is an aldosterone synthase inhibitor developed by Mineralys Therapeutics for high blood pressure. In clinical trials as an add-on medication for people with uncontrolled hypertension, decreased renin and elevated aldosterone it significantly reduced blood pressure. Hyperkalemia occurred in some trial ...
5) and aldosterone (C 21 H 28 O 5) (cortisone and aldosterone are isomers). The main corticosteroids produced by the adrenal cortex are cortisol and aldosterone. [1] The etymology of the cortico-part of the name refers to the adrenal cortex, which makes these steroid hormones. Thus a corticosteroid is a "cortex steroid". [citation needed]
It may be increased in 17α-hydroxylase deficiency, [4] in aldosterone synthase deficiency, [5] in primary aldosteronism, and may also indicate a histologic variant of the aldosteronoma. [4] Excessive secretion of 18-OH-DOC can cause mineralocorticoid excess syndrome, although these cases are very rare.
Aldosterone has effects on most or all cells of the body but, clinically, the most important actions are in the kidney, on cells of the late distal convoluted tubule and medullary collecting duct. In the principal cells aldosterone increases activity of basolateral membrane sodium-potassium ATPase and apical epithelial sodium channels, ENaC ...