Broadley K J
Division of Pharmacology, Welsh School of Pharmacy, University of Wales College of Cardiff, UK.
Acta Physiol Scand. 1990 Dec;140(4):481-9. doi: 10.1111/j.1748-1716.1990.tb09024.x.
The right superior of cervical sympathetic trunk of cats was sectioned preganglionically under anaesthesia. Six days later the blood pressure, heart rate and contractions of the left (control) and right (decentralized) nictitating membranes were recorded under chloralose anaesthesia (80 mg kg-1). The alpha-adrenoceptor-mediated contractile responses of the nictitating membrane to intravenous adrenaline were greater on the decentralized side than the control side, with a significant shift of the dose-response curve to the left. After phentolamine (8 mg kg-1 i.v.), adrenaline administered intra-arterially exerted beta-adrenoceptor-mediated relaxation of the nictitating membranes. However, there was no difference in the sensitivity or magnitude of responses between decentralized and control sides. In a separate series of experiments, the alpha-adrenoceptor-mediated contractile responses of the nictitating membrane to intra-arterial noradrenaline displayed supersensitivity on the decentralized side, the dose-response curve being significantly shifted to the left. In the same animals, the beta-adrenoceptor-mediated relaxation responses to intra-arterial isoprenaline were non-significantly greater on the decentralized side, presumably because of raised tone. However, when expressed as a percentage of the maximum relaxation, there was no difference in sensitivity. This study shows that the alpha-adrenoceptor-mediated contractile response of the nictitating membrane displays supersensitivity after preganglionic section of the sympathetic innervation. This is presumably because of an up-regulation arising from loss of sympathetic traffic onto the receptor. The relaxation response is mediated via adrenoceptors of the beta 2-subtype and shows no supersensitivity. This suggests that these receptors are not under the influence of the sympathetic innervation.
在麻醉状态下对猫的颈交感干右上级进行节前切断。六天后,在水合氯醛麻醉(80毫克/千克)下记录左(对照)、右(去神经支配)瞬膜的血压、心率和收缩情况。瞬膜对静脉注射肾上腺素的α-肾上腺素能受体介导的收缩反应在去神经支配侧比对照侧更大,剂量-反应曲线明显向左偏移。静脉注射酚妥拉明(8毫克/千克)后,动脉内注射肾上腺素可使瞬膜产生β-肾上腺素能受体介导的舒张。然而,去神经支配侧和对照侧在反应敏感性或幅度上没有差异。在另一系列实验中,瞬膜对动脉内去甲肾上腺素的α-肾上腺素能受体介导的收缩反应在去神经支配侧表现出超敏感性,剂量-反应曲线明显向左偏移。在同一动物中,去神经支配侧对动脉内异丙肾上腺素的β-肾上腺素能受体介导的舒张反应略大,但无统计学意义,可能是由于张力升高所致。然而,以最大舒张的百分比表示时,敏感性没有差异。本研究表明,交感神经节前切断后,瞬膜的α-肾上腺素能受体介导的收缩反应表现出超敏感性。这可能是由于受体上交感神经传入丧失导致的上调。舒张反应是通过β2-亚型肾上腺素能受体介导的,没有表现出超敏感性。这表明这些受体不受交感神经支配的影响。