Underlying mechanisms of urine storage dysfunction in rats with salt-loading hypertension
Underlying mechanisms of urine storage dysfunction in rats with salt-loading hypertension
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DOI：
10.1016/j.lfs.2015.09.010
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发表时间：
2015-11-15
期刊：
影响因子：
6.1
通讯作者：
Yokoyama, Osamu
中科院分区：
文献类型：
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作者：
Kurokawa, Tetsuyuki;Zha, Xinmin;Yokoyama, Osamu
目的：自发性高血压大鼠为探讨高血压相关尿液储存障碍的发病机制提供遗传学模型。然而，在人类中，高血压是由遗传和环境因素引起的，包括生活方式因素，如高卡路里饮食、过量盐分摄入和压力。本研究旨在探讨盐负荷对大鼠膀胱功能的影响及其与高盐相关的储藏功能障碍的可能机制。主要方法：6周龄雄性Dahl盐敏感(DS)和Dahl耐盐(DR)大鼠分别以正常和高盐饮食喂养12周。排尿参数从代谢笼中获得。取18周龄大鼠的整个膀胱，在脏器浴中扩张。测定扩张后膀胱上皮细胞三磷酸腺苷(ATP)和前列腺素E-2(PGE(2))的释放。用激光散斑血流成像系统测定膀胱血流量(BBF)的变化。主要发现：只有DS大鼠在盐负荷后平均血压(BP)升高。在非活动(睡眠)期间，喂食正常或高盐饮食的DR大鼠和正常饮食的DS大鼠每次排尿排尿量逐渐增加，而喂食高盐饮食的DS大鼠每次排尿排尿量没有变化。在喂食高盐饮食的DS大鼠中，膀胱扩张显著增加了尿路上皮的ATP和PGE(2)的释放。高盐饮食DS大鼠的BBF显著降低。意义：盐敏感型HT与尿液储存功能障碍之间关系的一个机制可能是通过抑制BBF增加尿路上皮释放的ATP和PGE(2)。(C)2015 Elsevier Inc.保留所有权利。
Aims: Spontaneous hypertensive rats provide a genetic model for exploring the pathogenesis of urine storage dysfunction related to hypertension (HT). In humans, however, HT develops by both genetic and environmental factors including lifestyle factors such as a high-calorie diet, excessive salt intake and stress. We investigated the influence of salt-loading on bladder function and the underlying mechanisms of storage dysfunction related to HT.Main methods: Six-week-old male Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats were fed with a normal or high-salt diet for 12 weeks. Micturition parameters were obtained from a metabolic cage. Whole bladders were excised from 18-week-old rats and distended in an organ bath. The releases of adenosine triphosphoric acid (ATP) and prostaglandin E-2 (PGE(2)) from the distended bladder epithelia were measured. Changes in bladder blood flow (BBF) were determined with a laser-speckle-blood-flow imaging system.Key findings: An increase in mean blood pressure (BP) was noted only in DS rats after salt-loading. During the inactive (sleeping) period, voided volume per micturition gradually increased in DR rats fed a normal or high-salt diet and normal-diet DS rats, while it did not change in the DS rats fed a high-salt diet. Bladder distension significantly increased ATP and PGE(2) release from the urothelium in DS rats fed a high-salt diet. BBF was significantly decreased in high-salt-diet DS rats.Significance: One mechanism behind the relationship between salt-sensitive HT and urine storage dysfunction may be an increase in ATP and PGE(2) release from the urothelium via suppression of BBF. (C) 2015 Elsevier Inc. All rights reserved.