Underlying mechanisms of urine storage dysfunction in rats with salt-loading hypertension

作者：Kurokawa Tetsuyuki; Zha Xinmin; Ito Hideaki; Aoki Yoshitaka; Akino Hironobu; Kobayashi Motohiro; Yokoyama Osamu^*

来源：Life Sciences, 2015, 141: 8-12.

DOI：10.1016/j.lfs.2015.09.010

• Bladder
• Storage dysfunction
• Rats
• Salt-loading hypertension
• Urothelium

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.

• 出版日期2015-11-15