期刊
CURRENT HYPERTENSION REPORTS
卷 14, 期 6, 页码 573-580出版社
SPRINGER
DOI: 10.1007/s11906-012-0297-0
关键词
Hypertension; Blood pressure; Aldosterone; Mineralocorticoid receptor; (MR); Glucocorticoids; Thiazides; Thiazide diuretics; Congestive heart failure; CHF; Primary aldosteronism; Obesity; Diabetes mellitus; Diabetic nephropathy; Cardiac fibrosis; Metabolic syndrome; Sympathetic nerve activation; Hyperkalemia
资金
- NHLBI NIH HHS [R01 HL027255] Funding Source: Medline
Mineralocorticoid receptors (MR) exist in many tissues, in which they mediate diverse functions crucial to normal physiology, including tissue repair and electrolyte and fluid homeostasis. However, inappropriate activation of MR within these tissues, and especially in the brain, causes hypertension and pathological vascular, cardiac, and renal remodeling. MR binds aldosterone, cortisol and corticosterone with equal affinity. In aldosterone-target cells, co-expression with the 11 beta-hydroxysteroid dehydrogenase 2 (HSD2) allows aldosterone specifically to activate MR. Aldosterone levels are excessive in primary aldosteronism, but in conditions with increased oxidative stress, like CHF, obesity and diabetes, MR may also be inappropriately activated by glucocorticoids. Unlike thiazide diuretics, MR antagonists are diuretics that do not cause insulin resistance. Addition of MR antagonists to standard treatment for hypertension and cardiac or renal disease decreases end-organ pathology and sympathetic nerve activation (SNA), and increases quality of life indices.
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