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 |
