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原发性高血压的病理生理学:最新进展

Pathophysiology of essential hypertension: an update.

作者信息

Saxena Tarun, Ali Azeema Ozefa, Saxena Manjari

机构信息

a Department of Internal Medicine , Mittal Hospital and Research Centre , Ajmer , India.

b Department Yoga and Physical education , Mittal Hospital and Research Centre , Ajmer , India.

出版信息

Expert Rev Cardiovasc Ther. 2018 Dec;16(12):879-887. doi: 10.1080/14779072.2018.1540301.

Abstract

Hypertension is caused by increased cardiac output and/or increased peripheral resistance. Areas covered: The various mechanisms affecting cardiac output/peripheral resistance involved in the development of essential hypertension are covered. These include genetics; sympathetic nervous system overactivity; renal mechanisms: excess sodium intake and pressure natriuresis; vascular mechanisms: endothelial cell dysfunction and the nitric oxide pathway; hormonal mechanisms: the renin-angiotensin-aldosterone system (RAAS); obesity, obstructive sleep apnea (OSA); insulin resistance and metabolic syndrome; uric acid; vitamin D; gender differences; racial, ethnic, and environmental factors; increased left ventricular ejection force and hypertension and its association with increased basal sympathetic activity - cortical connections. Expert commentary: Maximum association of hypertension is found with sympathetic overactivity which is directly or indirectly involved in different mechanisms of hypertension including RAAS, OSA, obesity, etc.. It is not overt sympathetic activity but disturbed basal sympathetic tone. Basal sympathetic tone arises from hypothalamus; possibly affected by cortical influences. Therefore, hypertension is not merely a disease of circulatory system alone. Its pathogenesis involves alteration in ANS (autonomic nervous system) and likely in cortical-hypothalamic connections. Assessment of ANS and cortical-hypothalamic connections may be required for better understanding of hypertension.

摘要

高血压是由心输出量增加和/或外周阻力增加引起的。涵盖领域:阐述了原发性高血压发生过程中影响心输出量/外周阻力的各种机制。这些机制包括遗传学;交感神经系统活性过高;肾脏机制:钠摄入过多与压力性利钠;血管机制:内皮细胞功能障碍与一氧化氮途径;激素机制:肾素 - 血管紧张素 - 醛固酮系统(RAAS);肥胖、阻塞性睡眠呼吸暂停(OSA);胰岛素抵抗与代谢综合征;尿酸;维生素D;性别差异;种族、民族和环境因素;左心室射血力增加与高血压及其与基础交感神经活动增加 - 皮质连接的关联。专家评论:高血压与交感神经活性过高关联最大,交感神经活性过高直接或间接参与高血压的不同机制,包括RAAS、OSA、肥胖等。并非明显的交感神经活动,而是基础交感神经张力紊乱。基础交感神经张力源于下丘脑;可能受皮质影响。因此,高血压不仅仅是循环系统的疾病。其发病机制涉及自主神经系统(ANS)的改变,可能还涉及皮质 - 下丘脑连接的改变。为更好地理解高血压,可能需要评估ANS和皮质 - 下丘脑连接。

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