Evaluation of a rat model of functional urinary bladder outlet obstruction produced by chronic inhibition of nitric oxide synthase

Publication date: Available online 15 August 2019Source: Life SciencesAuthor(s): Katsuhiko Noguchi, Kimio Sugaya, Saori Nishijima, Mayuko Sakanashi, Katsumi Kadekawa, Katsuhiro Ashitomi, Shiho Okitsu, Hideyuki YamamotoAbstractAimsLigation of the urethra to create partial bladder outlet obstruction has widely been used as an animal model of bladder obstruction, although obstructive bladder dysfunction may be due to both mechanical and functional obstruction. Previous studies in rodents have demonstrated that long-term nitric oxide (NO) deficiency can lead to detrusor overactivity, and lack of NO may thus cause impairment of bladder outlet relaxation. The aim of this study was to define the characteristics of bladder and urethral dysfunction induced by chronic NO deficiency through both in vivo and in vitro investigations.Main methodsRats were divided into two groups, and one group received an NO synthase inhibitor (Nω-nitro-L-arginine methyl ester hydrochloride: L-NAME) in the drinking water for 4 weeks. Bladder and urethral function were evaluated by continuous cystometry and isovolumetric cystometry. In vitro functional studies of detrusor strips and measurement of the mRNA and protein expression of an ischemic marker and a gap junction protein were also performed in separate rats.Key findingsL-NAME administration raised blood pressure and decreased plasma nitrite/nitrate level compared to the control group. L-NAME treatment increased the frequency of bladder contractions...
Source: Life Sciences - Category: Biology Source Type: research
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