期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1997
卷号：94
期号：26
页码：14848-14853
DOI：10.1073/pnas.94.26.14848
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Neuronal nitric oxide synthase (nNOS) generates NO in neurons, and heme-oxygenase-2 (HO-2) synthesizes carbon monoxide (CO). We have evaluated the roles of NO and CO in intestinal neurotransmission using mice with targeted deletions of nNOS or HO-2. Immunohistochemical analysis demonstrated colocalization of nNOS and HO-2 in myenteric ganglia. Nonadrenergic noncholinergic relaxation and cyclic guanosine 3',5' monophosphate elevations evoked by electrical field stimulation were diminished markedly in both nNOS{Delta}/{Delta} and HO-2{Delta}/{Delta} mice. In wild-type mice, NOS inhibitors and HO inhibitors partially inhibited nonadrenergic noncholinergic relaxation. In nNOS{Delta}/{Delta} animals, NOS inhibitors selectively lost their efficacy, and HO inhibitors were inactive in HO-2{Delta}/{Delta} animals.
