Cooper S M, McRitchie B
J Auton Pharmacol. 1985 Dec;5(4):325-31. doi: 10.1111/j.1474-8673.1985.tb00557.x.
The object of the study was to investigate the effects of dopamine receptor and alpha-adrenoreceptor agonists and antagonists on the gastric emptying of a liquid test meal in conscious rats and the possible involvement of these receptors in the mechanism of action of metoclopramide. The gastric emptying of a liquid test meal in conscious chronic gastric fistula rats was delayed following subcutaneous administration of either 6,7-ADTN (1-50 mg/kg) or clonidine (0.05-1 mg/kg). Phenylephrine (0.2-10 mg/kg s.c.) had no effect on gastric emptying, suggesting that dopamine and alpha 2-, but not alpha 1-adrenoreceptors may be involved in the control of gastric emptying in the rat. Phentolamine (0.2-5 mg/kg s.c.) and prazosin (0.1-0.5 mg/kg s.c.) potentiated the delay in gastric emptying induced by 6,7-ADTN, whilst yohimbine (1-5 mg/kg s.c.) and prazosin (0.1-0.5 mg/kg s.c.) reversed the delay in emptying induced by clonidine. All three alpha-adrenoreceptor antagonists also delayed gastric emptying in the absence of agonist. Propranolol (0.2-5 mg/kg s.c.) had no effect on either normal or delayed gastric emptying. Both metoclopramide (1-10 mg/kg s.c.) and haloperidol (0.02-0.5 mg/kg s.c.) reversed the 6,7-ADTN-induced delayed emptying but not the clonidine-induced delayed emptying. In addition, metoclopramide (5-10 mg/kg s.c.), but not haloperidol, increased gastric emptying in the absence of agonist. In conclusion, these results show that dopamine and alpha-adrenoreceptors may be involved in the control of gastric emptying in the rat. However, it would appear that alpha 2-adrenoreceptors are unlikely to be involved in the mechanism of action of metoclopramide.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是探讨多巴胺受体和α-肾上腺素能受体激动剂及拮抗剂对清醒大鼠液体试验餐胃排空的影响,以及这些受体在甲氧氯普胺作用机制中可能的参与情况。皮下注射6,7-ADTN(1-50毫克/千克)或可乐定(0.05-1毫克/千克)后,清醒慢性胃瘘大鼠的液体试验餐胃排空延迟。去氧肾上腺素(0.2-10毫克/千克皮下注射)对胃排空无影响,提示多巴胺和α2-,而非α1-肾上腺素能受体可能参与大鼠胃排空的控制。酚妥拉明(0.2-5毫克/千克皮下注射)和哌唑嗪(0.1-0.5毫克/千克皮下注射)增强了6,7-ADTN诱导的胃排空延迟,而育亨宾(1-5毫克/千克皮下注射)和哌唑嗪(0.1-0.5毫克/千克皮下注射)则逆转了可乐定诱导的排空延迟。所有三种α-肾上腺素能受体拮抗剂在无激动剂时也延迟胃排空。普萘洛尔(0.2-5毫克/千克皮下注射)对正常或延迟的胃排空均无影响。甲氧氯普胺(1-10毫克/千克皮下注射)和氟哌啶醇(0.02-0.5毫克/千克皮下注射)均逆转了6,7-ADTN诱导的排空延迟,但未逆转可乐定诱导的排空延迟。此外,甲氧氯普胺(5-10毫克/千克皮下注射),而非氟哌啶醇,在无激动剂时增加胃排空。总之,这些结果表明多巴胺和α-肾上腺素能受体可能参与大鼠胃排空的控制。然而,α2-肾上腺素能受体似乎不太可能参与甲氧氯普胺的作用机制。(摘要截短至250字)