Belan V, Macho L, Kvetnanský R, Machová J
J Auton Nerv Syst. 1982 Mar;5(2):119-33. doi: 10.1016/0165-1838(82)90033-9.
The effects of beta 1- and beta 2-selective and nonselective adrenergic agonists and antagonists were studied in the cat and rabbit superior cervical ganglion (SCG) in situ and in vitro. In experiments on the cat SCG in situ beta-adrenergic agonists induced an increase in positive afterpotential (PAP) of compound ganglionic action potential evoked by preganglionic stimulation in the following order of potency: isoprenaline (ISO) greater than salbutamol much greater than tazolol. Beta-adrenergic antagonists inhibited the ISO response in the following order of potency: propranolol greater than exaprolol much greater than H 35/25. Practolol did not exhibit beta-adrenergic blocking action; on the contrary, in higher doses it enhanced the response to ISO. In higher doses all beta-adrenergic antagonists tested depressed ganglionic transmission in an approximately similar range of doses. In experiments in vitro, using sucrose-gap technique. ISO induced depolarization of the cat SCG and this effect was inhibited in a dose-dependent manner by propranolol. Beta-adrenergic agonists did not induce depolarization of the rabbit SCG in experiments in situ and in vitro. The level of noradrenaline and dopamine in the cat and rabbit SCG did not differ significantly. Low level of adrenaline was found in the cat SCG; however, no adrenaline was detected in the rabbit SCG. No statistically significant change of cyclic AMP content was observed in the cat and rabbit SCG or in the incubation medium under conditions similar to those in which ISO induced depolarization of the cat SCG. It is concluded that the beta-adrenergic receptors present in the cat SCG resemble the beta 2-subtype and that the presence of an electrophysiologic response to beta-adrenergic agonists appears to be species-dependent. The depolarization of the cat SCG due to beta-adrenergic receptor stimulation is not coupled with cyclic AMP increase.
在猫和兔的颈上神经节(SCG)原位及体外研究了β1和β2选择性及非选择性肾上腺素能激动剂和拮抗剂的作用。在猫SCG原位实验中,β肾上腺素能激动剂可使节前刺激诱发的复合神经节动作电位的正后电位(PAP)增加,其效力顺序为:异丙肾上腺素(ISO)>沙丁胺醇>噻唑洛尔。β肾上腺素能拮抗剂抑制ISO反应的效力顺序为:普萘洛尔>心得舒>H 35/25。醋丁洛尔未表现出β肾上腺素能阻断作用;相反,高剂量时它增强了对ISO的反应。高剂量时,所有测试的β肾上腺素能拮抗剂在大致相似的剂量范围内抑制神经节传递。在体外实验中,使用蔗糖间隙技术,ISO使猫SCG去极化,且这种作用被普萘洛尔以剂量依赖性方式抑制。在原位和体外实验中,β肾上腺素能激动剂未使兔SCG去极化。猫和兔SCG中去甲肾上腺素和多巴胺水平无显著差异。在猫SCG中发现肾上腺素水平较低;然而,在兔SCG中未检测到肾上腺素。在与ISO使猫SCG去极化的条件相似的情况下,猫和兔SCG或孵育培养基中未观察到环磷酸腺苷(cAMP)含量有统计学显著变化。结论是猫SCG中存在的β肾上腺素能受体类似于β2亚型,并且对β肾上腺素能激动剂的电生理反应似乎具有种属依赖性。β肾上腺素能受体刺激导致的猫SCG去极化与cAMP增加无关。