INTRINSIC CARDIAC NEURONS INVOLVED IN CARDIAC REGULATION POSSESS ALPHA(1)-ADRENOCEPTORS, ALPHA(2)-ADRENOCEPTORS, BETA(1)-ADRENOCEPTORS AND BETA(2)-ADRENOCEPTORS

Authors
Citation
Ja. Armour, INTRINSIC CARDIAC NEURONS INVOLVED IN CARDIAC REGULATION POSSESS ALPHA(1)-ADRENOCEPTORS, ALPHA(2)-ADRENOCEPTORS, BETA(1)-ADRENOCEPTORS AND BETA(2)-ADRENOCEPTORS, Canadian journal of cardiology, 13(3), 1997, pp. 277-284
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
0828282X
Volume
13
Issue
3
Year of publication
1997
Pages
277 - 284
Database
ISI
SICI code
0828-282X(1997)13:3<277:ICNIIC>2.0.ZU;2-D
Abstract
OBJECTIVE: To determine whether intrinsic cardiac neurons involved in cardiac regulation possess alpha(1)-, alpha(2)-, beta(1)- or beta(2)-a drenoceptors. DESIGN: The alpha(1)-adrenoceptor agonist phenylephrine, the alpha(2)-adrenoceptor agonist clonidine, the beta(1)-adrenoceptor agonist prenaterol and the beta(2)-adrenoceptor agonist terbutaline w ere administered individually to a population of spontaneously active intrinsic cardiac neurons either locally (10 mu L of 100 mu M solution ; eight dogs) or via the local arterial blood supply (0.1 mL of 100 mu M solution; 20 dogs) in artificially ventilated, open chest anestheti zed dogs. Neuronal and cardiac effects induced by each of the adrenerg ic agonists were also tested in the presence of an antagonist selectiv e to each adrenoceptor subtype studied. MAIN RESULTS: The activity of intrinsic cardiac neurons was modified by at least one of the adrenoce ptor agonists tested, and 34% of the spontaneously active neurons were affected by all four agonists. Alpha-adrenoceptor agonists either inc reased or decreased neuronal activity, depending on the population of neurons studied. On the other hand, the activity generated by intrinsi c cardiac neurons was augmented by beta-adrenoceptor agonists. Ventric ular contractile force increased when intrinsic cardiac neurons were e xcited by adrenoceptor agonists. The spontaneous activity generated by neurons was suppressed by beta-adrenoceptor, but not alpha-adrenocept or, blockade. Neuronal and cardiovascular responses were no longer eli cited by an agonist in the presence of its selective antagonist; they were elicited in the presence of antagonists to the other receptor sub types studied. CONCLUSIONS: Intrinsic cardiac neurons involved in card iac regulation possess alpha(1)-, alpha(2)-, beta(1)- or beta(2)-adren oceptors. Intrinsic cardiac adrenergic neurons receive tonic inputs vi a beta-, but not alpha-, adrenoceptors. These data indicate that adren ergic blockade may affect cardiac function, in part, via modification of the intrinsic cardiac nervous system.