Yoshida-Yoneda E, O-Lee T J, Wei J Y, Vigna S R, Taché Y
Center for Ulcer Research and Education/Digestive Disease Research Center, West Los Angeles Veterans Affairs Medical Center, California 90073, USA.
Am J Physiol. 1996 Dec;271(6 Pt 2):R1584-93. doi: 10.1152/ajpregu.1996.271.6.R1584.
Bombesin's influence on gastric vagal afferent discharge (GVAD) was studied in urethan-anesthetized rats. Vehicle and peptides were injected intravenously at 30-min intervals. Cholecystokinin (CCK; 300 pmol) and bombesin (300 pmol) increased ongoing multiunit GVAD by 153 +/- 59 and 162 +/- 37%, respectively; similar increases were induced by a second injection of bombesin and CCK. The bombesin antagonist, ICI-216140, prevented bombesin-induced increase in GVAD, whereas the CCK response was not influenced. The CCK-A receptor antagonist devazepide reduced the activation of GVAD induced by bombesin from 107 +/- 11 to 63 +/- 6%, while abolishing the CCK response. Devazepide given alone or in combination with ICI-216140 did not modify gastric distension (3 ml)-induced increase in GVAD. Of 22 single units that were activated by gastric load (4 ml), 17 and 20 units responded also to bombesin (620 pmol) and CCK (870 pmol), respectively. Of the nine units that did not respond to gastric load, eight had an increase in GVAD induced by both bombesin and CCK. There was no specific binding of 125I-labeled [Tyr4]bombesin on cervical vagus, either intact or 24 h after ligation. These data suggest that intravenous bombesin-induced stimulation of GVAD is indirect and initially mediated through specific receptor activation influencing gastric smooth muscle and the release of CCK.
在乌拉坦麻醉的大鼠中研究了蛙皮素对胃迷走神经传入放电（GVAD）的影响。以30分钟的间隔静脉注射赋形剂和肽。胆囊收缩素（CCK；300 pmol）和蛙皮素（300 pmol）分别使持续的多单位GVAD增加153±59%和162±37%；第二次注射蛙皮素和CCK也诱导了类似的增加。蛙皮素拮抗剂ICI-216140可阻止蛙皮素诱导的GVAD增加，而CCK反应不受影响。CCK-A受体拮抗剂地伐西匹将蛙皮素诱导的GVAD激活从107±11%降低至63±6%，同时消除了CCK反应。单独给予地伐西匹或与ICI-216140联合使用均未改变胃扩张（3 ml）诱导的GVAD增加。在被胃负荷（4 ml）激活的22个单单位中，分别有17个和20个单位也对蛙皮素（620 pmol）和CCK（870 pmol）有反应。在对胃负荷无反应的9个单位中，有8个单位的GVAD因蛙皮素和CCK均增加。在完整的或结扎后24小时的颈迷走神经上，未发现125I标记的[酪氨酸4]蛙皮素的特异性结合。这些数据表明，静脉注射蛙皮素诱导的GVAD刺激是间接的，最初是通过影响胃平滑肌和CCK释放的特异性受体激活介导的。
