Unno T, Shingu H, Isogai M, Komori S, Ohashi H
Department of Veterinary Medicine, Faculty of Agriculture, Gifu University, Japan.
J Vet Med Sci. 1998 Nov;60(11):1227-32. doi: 10.1292/jvms.60.1227.
Effect of neurotensin (NT) on carbachol(CCh)-induced tension development due to Ca2+ release from intracellular stores was investigated in beta-escin-skinned smooth muscle of guinea-pig ileum. NT (10 nM) increased the tension development in response to CCh. NT also increased the tension response to caffeine, another store-Ca2+ releaser. NT did not exert such an effect in pertusis toxin (PTX)-treated preparations. Treatment with isoprenaline to elevate endogenous cyclic AMP levels or with dibutyryl cyclic AMP did not affect the effect of NT. A nonpeptide NT antagonist, SR 48692, failed to block the effect of NT. NT shifted the pCa-tension relationship in the lower direction of Ca2+ concentration. NT was incapable of releasing Ca2+ from intracellular stores. The results suggest that NT may cause an increase in Ca2+ sensitivity of contractile elements to potentiate the CCh-induced tension development due to release of stored Ca2+ and that the effect is mediated by SR 48692-insensitive NT receptors linked to a PTX-sensitive G protein which works with no relation to a change in cytosolic cyclic AMP levels.
在豚鼠回肠的β-七叶皂苷去表皮平滑肌中，研究了神经降压素（NT）对因细胞内钙库释放Ca2+而引起的卡巴胆碱（CCh）诱导的张力发展的影响。NT（10 nM）增加了对CCh的张力发展。NT还增加了对另一种钙库释放剂咖啡因的张力反应。NT在百日咳毒素（PTX）处理的标本中未产生这种作用。用异丙肾上腺素提高内源性环磷酸腺苷水平或用二丁酰环磷酸腺苷处理均不影响NT的作用。一种非肽类NT拮抗剂SR 48692未能阻断NT的作用。NT使pCa-张力关系向较低的Ca2+浓度方向移动。NT不能从细胞内钙库释放Ca2+。结果表明，NT可能会导致收缩元件对Ca2+的敏感性增加，从而增强因储存的Ca2+释放而引起的CCh诱导的张力发展，并且该作用由与PTX敏感的G蛋白相连的SR 48692不敏感的NT受体介导，该G蛋白的作用与胞质环磷酸腺苷水平的变化无关。
