Intrinsic cardiac neurons involved in cardiac regulation possess alpha 1-, alpha 2-, beta 1- and beta 2-adrenoceptors.
OBJECTIVE
To determine whether intrinsic cardiac neurons involved in cardiac regulation possess alpha 1-, alpha 2-, beta 1-, or beta 2-adrenoceptors.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Armour
J A
JA
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia. jarmour@is.dal.ca
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D005260:Female; D008297:Male; D009206:Myocardium / Q000166:cytology*; D009474:Neurons / Q000737:chemistry* / Q000187:drug effects*; D010656:Phenylephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000032:analysis* / Q000187:drug effects*; D018340:Receptors, Adrenergic, alpha-1 / Q000032:analysis / Q000187:drug effects; D018341:Receptors, Adrenergic, alpha-2 / Q000032:analysis / Q000187:drug effects; D011943:Receptors, Adrenergic, beta / Q000032:analysis* / Q000187:drug effects*; D018342:Receptors, Adrenergic, beta-1 / Q000032:analysis / Q000187:drug effects; D018343:Receptors, Adrenergic, beta-2 / Q000032:analysis / Q000187:drug effects; D013726:Terbutaline / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011942:Receptors, Adrenergic, alpha; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D011943:Receptors, Adrenergic, beta; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D010656:Phenylephrine; D013726:Terbutaline