Hypertension (HTN) is a primary risk factor for cardiovascular (CV) events, target organ damage (TOD), premature death and disability worldwide. The pathophysiology of HTN is complex and influenced by many factors including biological sex. Studies show that the prevalence of HTN is higher among adults aged 60 and over, highlighting the increase of HTN after menopause in women. Estrogen (E2) plays an important role in the development of systemic HTN and TOD, exerting several modulatory effects. The influence of E2 leads to alterations in mechanisms regulating the sympathetic nervous system, renin-angiotensin-aldosterone system, body mass, oxidative stress, endothelial function and salt sensitivity; all associated with a crucial inflammatory state and influenced by genetic factors, ultimately resulting in cardiac, vascular and renal damage in HTN. In the present article, we discuss the role of E2 in mechanisms accounting for the development of HTN and TOD in a sex-specific manner. The identification of targets with therapeutic potential would contribute to the development of more efficient treatments according to individual needs.

中文翻译：

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高血压性别差异及靶器官损害的雌激素相关机制。

高血压 (HTN) 是全世界心血管 (CV) 事件、靶器官损伤 (TOD)、过早死亡和残疾的主要危险因素。HTN的病理生理学很复杂，受包括生物性别在内的多种因素影响。研究表明，60 岁及以上成年人的高血压患病率较高，凸显了女性绝经后高血压的增加。雌激素 (E2) 在全身性 HTN 和 TOD 的发展中发挥着重要作用，发挥多种调节作用。E2的影响导致交感神经系统、肾素-血管紧张素-醛固酮系统、体重、氧化应激、内皮功能和盐敏感性调节机制的改变；所有这些都与关键的炎症状态有关，并受到遗传因素的影响，最终导致高血压患者的心脏、血管和肾脏损伤。在本文中，我们讨论了 E2 在以性别特异性方式解释 HTN 和 TOD 发展的机制中的作用。识别具有治疗潜力的靶点将有助于根据个人需求开发更有效的治疗方法。