作者: s. iino , k. horiguchi , y. nojyo , s. m. ward , k. m. sanders
DOI: 10.1111/J.1365-2982.2008.01236.X
关键词:
摘要: Nitric oxide (NO) is an inhibitory signalling molecule in the gastrointestinal (GI) tract that released from neurons and leucocytes during inflammation. NO stimulates soluble guanylate cyclase (sGC), elevates cyclic guanosine 3′,5′-monophospate (cGMP), subsequently activates cGMP-dependent protein kinase (PKG). Targets for guinea pig caecum were investigated by characterizing cellular distribution of sGC, cGMP PKG. Immunoreactivity both isoforms sGCα1 sGCβ1, was observed interstitial cells Cajal (ICC) enteric tunica muscularis. Double labelling with anti-Kit anti-sGC antibodies showed sGCβ1-like immunoreactivity (LI) almost all intramuscular (IM) myenteric ICC. Neuronal processes neuronal synthase closely apposed to ICC expressing sGC-LI. Cells sGC-LI possessed ultrastructural features ICC-IM: caveolae, close association nerve bundles contacts smooth muscle (SMC). Sodium nitroprusside, added phosphodiesterase inhibitors (3-isobutyl-1-methylxanthine zaprinast), enhanced cGMP-LI some neurons. Nerve stimulation also increased In contrast, no resolvable increase any when sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one present. SMC expressed PKG type I-LI. These data show express downstream molecules necessary transduce nitrergic signals activate pathways thus are primary targets other GI tract.