Armour J A
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia.
Can J Cardiol. 1997 Mar;13(3):277-84.
To determine whether intrinsic cardiac neurons involved in cardiac regulation possess alpha 1-, alpha 2-, beta 1-, or beta 2-adrenoceptors.
The alpha1-adrenoceptor agonist phenylephrine, the alpha 2-adrenoceptor agonist clonidine, the beta 1-adrenoceptor agonist prenaterol and the beta 2-adrenoceptor agonist terbutaline were administered individually to a population of spontaneously active intrinsic cardiac neurons either locally (10 microL of 100 microM solution; eight dogs) or via the local arterial blood supply (0.1 mL of 100 microM solution; 20 dogs) in artificially ventilated, open chest anesthetized dogs. Neuronal and cardiac effects induced by each of the adrenergic agonists were also tested in the presence of an antagonist selective to each adrenoceptor subtype studied.
The activity of intrinsic cardiac neurons was modified by at least one of the adrenoceptor agonists tested, and 34% of the spontaneously active neurons were affected by all four agonists. Alpha-adrenoceptor agonists either increased or decreased neuronal activity, depending on the population of neurons studied. On the other hand, the activity generated by intrinsic cardiac neurons was augmented by beta-adrenoceptor agonists. Ventricular contractile force increased when intrinsic cardiac neurons were excited by adrenoceptor agonists. The spontaneous activity generated by neurons was suppressed by beta-adrenoceptor, but not alpha-adrenoceptor, blockade. Neuronal and cardiovascular responses were no longer elicited by an agonist in the presence of its selective antagonist; they were elicited in the presence of antagonists to the other receptor subtypes studied.
Intrinsic cardiac neurons involved in cardiac regulation possess alpha 1-, alpha 2-, beta 1- or beta 2-adrenoceptors. Intrinsic cardiac adrenergic neurons receive tonic inputs via beta-, but not alpha-, adrenoceptors. These data indicate that adrenergic blockade may affect cardiac function, in part, via modification of the intrinsic cardiac nervous system.
确定参与心脏调节的心脏内在神经元是否具有α1、α2、β1或β2肾上腺素能受体。
将α1肾上腺素能受体激动剂去氧肾上腺素、α2肾上腺素能受体激动剂可乐定、β1肾上腺素能受体激动剂普瑞特罗和β2肾上腺素能受体激动剂特布他林分别局部（10微升100微摩尔溶液；8只犬）或通过局部动脉血供应（0.1毫升100微摩尔溶液；20只犬）给予人工通气、开胸麻醉犬的一群自发活动的心脏内在神经元。在存在对所研究的每种肾上腺素能受体亚型具有选择性的拮抗剂的情况下，还测试了每种肾上腺素能激动剂诱导的神经元和心脏效应。
所测试的至少一种肾上腺素能受体激动剂改变了心脏内在神经元的活性，并且34%的自发活动神经元受到所有四种激动剂的影响。α肾上腺素能受体激动剂根据所研究的神经元群体增加或降低神经元活性。另一方面，β肾上腺素能受体激动剂增强了心脏内在神经元产生的活性。当心脏内在神经元被肾上腺素能受体激动剂兴奋时，心室收缩力增加。神经元产生的自发活动被β肾上腺素能受体阻断，但不被α肾上腺素能受体阻断所抑制。在存在其选择性拮抗剂的情况下，激动剂不再引发神经元和心血管反应；在存在针对所研究的其他受体亚型的拮抗剂的情况下，它们会引发反应。
参与心脏调节的心脏内在神经元具有α1、α2、β1或β2肾上腺素能受体。心脏内在肾上腺素能神经元通过β肾上腺素能受体而非α肾上腺素能受体接受紧张性输入。这些数据表明，肾上腺素能阻断可能部分通过改变心脏内在神经系统来影响心脏功能。
