pubmed:abstractText |
NO released by myenteric neurons controls the off contraction induced by electrical field stimulation (EFS) in distal esophageal smooth muscle, but in the presence of nitric oxide synthase (NOS) inhibitor, L-NAME, contraction by EFS occurs at the same time. The authors investigated the intracellular signaling pathways related with G protein and ionic channel EFS-induced contraction using cat esophageal muscles. EFS-induced contractions were significantly suppressed by tetrodotoxin (1 microM) and atropine (1 microM). Furthermore, nimodipine inhibited both on and off contractions by EFS in a concentration dependent meaner. The characteristics of 'on' and 'off' contraction and the effects of G-proteins, phospholipase, and K(+) channel on EFS-induced contraction in smooth muscle were also investigated. Pertussis toxin (PTX, a G(i) inactivator) attenuated both EFS-induced contractions. Cholera toxin (CTX, G(s) inactivator) also decreased the amplitudes of EFS-induced off and on contractions. However, phospholipase inhibitors did not affect these contractions. Pinacidil (a K(+) channel opener) decreased these contractions, and tetraethylammonium (TEA, K(+) (Ca) channel blocker) increased them. These results suggest that EFS-induced on and off contractions can be mediated by the activations Gi or Gs proteins, and that L-type Ca(2+) channel may be activated by G-protein alpha subunits. Furthermore, K(+) (Ca)-channel involve in the depolarization of esophageal smooth muscle. Further studies are required to characterize the physiological regulation of Ca(2+) channel and to investigate the effects of other K(+) channels on EFS-induced on and off contractions.
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