Role of estrogen in diastolic dysfunction.

摘要: The prevalence of left ventricular diastolic dysfunction (LVDD) sharply increases in women after menopause and may lead to heart failure. While evidence suggests that estrogens protect the premenopausal from hypertension remodeling, specific mechanisms involved remain elusive. Moreover, whether there is a protective role against cardiovascular disease, specifically LVDD, continues be controversial. Clinical basic science have implicated activation renin-angiotensin-aldosterone system (RAAS), linked loss ovarian estrogens, pathogenesis postmenopausal dysfunction. As consequence increased tissue ANG II low estrogen, maladaptive nitric oxide synthase (NOS) produces ROS contribute female sex-specific hypertensive disease. Recent insights rodent models mimic cardiac phenotype an estrogen-insufficient or -deficient woman (e.g., premature failure postmenopausal), including ovariectomized congenic mRen2.Lewis rat, provide showing estrogen modulates RAAS NOS related intracellular signaling pathways, part via membrane G protein-coupled receptor 30 (GPR30; also called 1). Complementing research this field, echocardiographic correlates LVDD as well inherent limitations its use preclinical studies will briefly presented. Understanding roles GPR30, their interactions with local system, relationship each these necessary identify new therapeutic targets alternative treatments for achieve benefits replacement without side effects contraindications.