期刊
SURGERY
卷 130, 期 2, 页码 236-241出版社
MOSBY, INC
DOI: 10.1067/msy.2001.115903
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资金
- NIDDK NIH HHS [5F32-DK-09834, DK-43899] Funding Source: Medline
Background. Previous studies have demonstrated that an antagonist of nitric oxide synthase inhibits neurally mediated chloride secretion in response to serotonin (5-HT). The purpose of this study was to demonstrate that chloride secretion in rat colonocytes that were caused by stimulation of neural. 5-HT receptors is mediated by way of a nitrergic pathway that involves the activation of guanylate cyclase. Methods. The nitric oxide (NO) donor, diethylenetriamine/NO (DNO), was added to an enriched suspension of rat colonocytes that were preloaded with Cl-36(-). In Parallel experiments, DNO (1 mu mol/L) was added to cells that were Preheated with the specific inhibitor of soluble guanylate cyclase, NS2028 (2 mu mol/L). In additional studies, the neural 5-HT3 receptor agonist, 2-methyl-5-HT (10 mu mol/L), was added to the serosal surface of muscle-stripped sheets of rat colonic mucosa that were mounted in Ussing chambers under voltage clamp conditions, both in the absence and presence of NS2028 (20 mum). Results. DNO induced 18.0% +/-8.0%greater Cl-36(-) efflux than controls (P<.05; n = 14 animals). This efflux was abolished by previous treatment with NS2028. In the chamber experiments, 2-methyl-5-HT induced electrogenic chloride secretion that was significantly inhibited by previous treatment with NS2028 (2.20.5 muA/cm(2) vs 13.1 +/-2.1 muA/cm(2); P<.001; n = 9 animals). Conclusions. The predominant secretomotor neurotransmitter that mediates the chloride secretory effects of 5-HT in vitro is nitric oxide. Both the secretory effect initiated at the 5-HT3 receptor on enteric neurons and at the NO- receptor on the rat colonocytes are mediated through the activation of intracellular guanylate cyclase and the production of cyclic guanosine monophosphate.
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