Andrea Vecchiola, Thomas Uslar, Isidora Friedrich, Joaquin Aguirre, Alejandra Sandoval, Cristian A Carvajal, Alejandra Tapia-Castillo, Alejandra Martínez-García, Carlos E Fardella
{"title":"The role of sex hormones in aldosterone biosynthesis and their potential impact on its mineralocorticoid receptor.","authors":"Andrea Vecchiola, Thomas Uslar, Isidora Friedrich, Joaquin Aguirre, Alejandra Sandoval, Cristian A Carvajal, Alejandra Tapia-Castillo, Alejandra Martínez-García, Carlos E Fardella","doi":"10.1097/XCE.0000000000000305","DOIUrl":null,"url":null,"abstract":"<p><p>Blood pressure (BP) regulation is a complex process involving various hormones, including aldosterone and its mineralocorticoid receptor. Mineralocorticoid receptor is expressed in several tissues, including the kidney, and plays a crucial role in regulating BP by controlling the sodium and water balance. During different stages of life, hormonal changes can affect mineralocorticoid receptor activity and aldosterone levels, leading to changes in BP. Increasing evidence suggests that sex steroids modulate aldosterone levels. Estrogens, particularly estradiol, mediate aldosterone biosynthesis by activating classical estrogen receptors and the G protein-coupled receptor. Progesterone acts as an anti-mineralocorticoid by inhibiting the binding of aldosterone to the mineralocorticoid receptor. Moreover, progesterone inhibits aldosterone synthase enzymes. The effect of testosterone on aldosterone synthesis is still a subject of debate. However, certain studies show that testosterone downregulates the mRNA levels of aldosterone synthase, leading to decreased plasma aldosterone levels.</p>","PeriodicalId":43231,"journal":{"name":"Cardiovascular Endocrinology & Metabolism","volume":null,"pages":null},"PeriodicalIF":1.3000,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11155591/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular Endocrinology & Metabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/XCE.0000000000000305","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Blood pressure (BP) regulation is a complex process involving various hormones, including aldosterone and its mineralocorticoid receptor. Mineralocorticoid receptor is expressed in several tissues, including the kidney, and plays a crucial role in regulating BP by controlling the sodium and water balance. During different stages of life, hormonal changes can affect mineralocorticoid receptor activity and aldosterone levels, leading to changes in BP. Increasing evidence suggests that sex steroids modulate aldosterone levels. Estrogens, particularly estradiol, mediate aldosterone biosynthesis by activating classical estrogen receptors and the G protein-coupled receptor. Progesterone acts as an anti-mineralocorticoid by inhibiting the binding of aldosterone to the mineralocorticoid receptor. Moreover, progesterone inhibits aldosterone synthase enzymes. The effect of testosterone on aldosterone synthesis is still a subject of debate. However, certain studies show that testosterone downregulates the mRNA levels of aldosterone synthase, leading to decreased plasma aldosterone levels.
血压(BP)调节是一个复杂的过程,涉及多种激素,包括醛固酮及其矿质皮质激素受体。矿质皮质激素受体在包括肾脏在内的多个组织中表达,通过控制钠和水的平衡在调节血压方面发挥着重要作用。在生命的不同阶段,荷尔蒙的变化会影响矿质皮质激素受体的活性和醛固酮水平,从而导致血压变化。越来越多的证据表明,性类固醇可调节醛固酮水平。雌激素,尤其是雌二醇,通过激活经典的雌激素受体和 G 蛋白偶联受体,介导醛固酮的生物合成。黄体酮通过抑制醛固酮与矿质皮质激素受体的结合,起到抗矿质皮质激素的作用。此外,孕酮还能抑制醛固酮合成酶。睾酮对醛固酮合成的影响仍存在争议。不过,某些研究表明,睾酮会下调醛固酮合成酶的 mRNA 水平,导致血浆中醛固酮水平下降。