Abstract：
In men, the lower urinary tract comprises the urinary bladder, urethra, and prostate, and its primary functions include urine storage and voiding. Hypertension is a condition that causes multi-organ damage and an age-dependent condition. Hypertension and the renin-angiotensin system activation are associated with the development of lower urinary tract dysfunction. Hypertensive animal models show bladder dysfunction, urethral dysfunction, and prostatic hyperplasia. In the renin-angiotensin system, angiotensin II and the angiotensin II type 1 receptor, which are expressed in the lower urinary tract, have been implicated in the pathogenesis of lower urinary tract dysfunction. Moreover, among the several antihypertensives, renin-angiotensin system inhibitors have proven effective in human and animal models of lower urinary tract dysfunction. This review aimed to elucidate the hitherto known mechanisms underlying the development of lower urinary tract dysfunction in relation to hypertension and the angiotensin II/angiotensin II type 1 receptor axis and the effect of renin-angiotensin system inhibitors on lower urinary tract dysfunction. Possible mechanisms through which hypertension or activation of Ang II/AT1 receptor axis causes LUTD such as bladder dysfunction, urethral dysfunction, and prostatic hyperplasia. LUT: lower urinary tract, LUTD: lower urinary tract dysfunction, AT1: angiotensin II type 1, ACE: angiotensin-converting enzyme.
摘要：
在男人中，下尿路包括膀胱，尿道,前列腺，其主要功能包括尿液储存和排尿。高血压是一种导致多器官损伤和年龄依赖性疾病的疾病。高血压和肾素-血管紧张素系统激活与下尿路功能障碍的发展有关。高血压动物模型显示膀胱功能障碍，尿道功能障碍,前列腺增生.在肾素-血管紧张素系统中，血管紧张素II和血管紧张素II1型受体，在下尿路表达，与下尿路功能障碍的发病机制有关。此外，在几种降压药中，肾素-血管紧张素系统抑制剂已被证明在下尿路功能障碍的人类和动物模型中有效。这篇综述旨在阐明迄今为止与高血压和血管紧张素II/血管紧张素II1型受体轴相关的下尿路功能障碍发展的已知机制，以及肾素-血管紧张素系统抑制剂对下尿路功能障碍的影响。高血压或AngII/AT1受体轴激活导致LUTD的可能机制，如膀胱功能障碍，尿道功能障碍,前列腺增生.LUT：下尿路，LUTD：下尿路功能障碍，AT1：血管紧张素II1型，ACE：血管紧张素转换酶。
