Publications of Faculty of Medicine:Role of L-Arginine-Nitric Oxide (NO) Pathway in the Regulation of Gall Bladder Motility: Abstract

Role of L-Arginine-Nitric Oxide (NO) Pathway in the Regulation of Gall Bladder Motility
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Over the past few years, nitric oxide (NO) has been found to be an important mediator for neural, cardiovascular and gastrointestinal functions. The present study aimed to investigate the role of L-arginine-NO pathway in gall bladder motility. The whole gall bladders of twenty adult male guinea pigs were used in this study. Carbacol (2μg/m1) was used as a contractile agonist. L-arginine, NO-precursor, in a dose of 0.5me/m1 caused a significant reduction of carbacol-induced contraction. L-NAME, NO synthase (NOS) inhibitor, in a dose of 251.1g/m1 caused a significant potentiation of carbacol-induced contraction of gall bladder. The inhibitory effect of L-arginine was abolished in the presence of L-NAME (25μg/m1) or methylene blue (guanylate cy_elase inactivator) in a dose of 20p.g/ml. In addition, sodium nitroprusside (SNP), which is an exogenous NO-donor, in a dose of 10;20,404ml, caused a significant and dosedependent relaxation of gall bladder precontracted by carbacol. The abilit‘ of L-NAME to abolish the inhibitory effect of L-arginine and the relaxant effect of SNP indicated that L-aruinine-NO pathway may participate in the regulatory mechanisms of gall bladder motility. The ability of methylene blue to abolish the inhibitory effect of NO-precursor, L-arginine, indicated that NO-relaxing effect may be due to activation of guanylate cyclase enzyme. The use of NO-donors in the treatment of acute biliary colic could be recommended. However, the use of NO-donors for a long time may cause an impairment of gall bladder motility and cholelithiasis