Rodríguez-Sinovas A, Fernández E, Goñalons E
Physiology Unit, Veterinary Faculty, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Life Sci. 1996;58(21):1869-82. doi: 10.1016/0024-3205(96)00152-x.
In chickens CCK-8s induces defecation and causes an inhibition of rectal electrical activity (EA) and an increase in cecal motility. In contrast, CCK-4 inhibits the motility of both rectum and ceca. The cecorectal responses to CCK-8s and CCK-4, given intravenously (i.v.), were studied in conscious chickens prepared with electrodes for electromyography; the influence of atropine, phentolamine plus propranolol, hexamethonium and L-NAME on such responses was determined. Atropine and phentolamine plus propranolol did not cause any change in the response to CCK-8s or CCK-4 in the cecorectal area. Hexamethonium only induced a significant decrease in the number of defecations (ND) induced by CCK-8s. L-NAME slightly modified the decrease in rectal EA due to CCK-8s. The effects of intracerebroventricular (i.c.v.) administration of CCK-8s and CCK-4 were also studied. CCK-8s and CCK-4, given i.c.v., caused, in conscious chickens, a slight decrease in cecal EA, in the 15 minutes following administration. This effect was similar to that seen after i.v. administration of CCK-4. In conclusion, our results suggest that the inhibitory action of CCK on chicken rectum is mediated, at least in part, through nitric oxide release. In addition, nicotinic receptors mediate the increase in the ND caused by CCK-8s. Ganglionic, muscarinic, adrenergic and nitrergic blockade were not able to modify the excitatory cecal response to CCK-8s, which may indicate that the receptor mediating this effect is located on the cecal smooth muscle. Finally, the inhibitory action of i.v. CCK-4 on chicken cecum seems to be centrally mediated, as suggested by the fact that i.c.v. administration of either CCK-8s or CCK-4 induce a similar effect.
在鸡体内，CCK-8s可诱发排便，并导致直肠电活动（EA）受到抑制，盲肠蠕动增强。相比之下，CCK-4可抑制直肠和盲肠的蠕动。本研究在清醒的鸡身上进行，这些鸡已植入电极用于肌电图记录，通过静脉注射（i.v.）给予CCK-8s和CCK-4，研究其对盲肠和直肠的反应；同时测定阿托品、酚妥拉明加普萘洛尔、六甲铵和L-NAME对这些反应的影响。阿托品以及酚妥拉明加普萘洛尔对CCK-8s或CCK-4在盲肠直肠区域的反应未产生任何改变。六甲铵仅使CCK-8s诱发的排便次数（ND）显著减少。L-NAME对CCK-8s所致的直肠EA降低仅有轻微影响。还研究了脑室内（i.c.v.）注射CCK-8s和CCK-4的效果。在清醒鸡中，脑室内注射CCK-8s和CCK-4后15分钟内，会导致盲肠EA略有下降。此效应与静脉注射CCK-4后所见效应相似。总之，我们的结果表明，CCK对鸡直肠的抑制作用至少部分是通过一氧化氮释放介导的。此外，烟碱受体介导了CCK-8s引起的ND增加。神经节、毒蕈碱、肾上腺素能和一氧化氮能阻滞剂均无法改变CCK-8s对盲肠的兴奋性反应，这可能表明介导此效应的受体位于盲肠平滑肌上。最后，静脉注射CCK-4对鸡盲肠的抑制作用似乎是由中枢介导的，因为脑室内注射CCK-8s或CCK-4均可诱导类似效应。
