Intrathoracic ganglionic beta-adrenergic receptors involved in efferent sympathetic regulation of the canine heart.

The enhancement of cardiac inotropism induced by electrical stimulation of acutely decentralized efferent preganglionic sympathetic axons was reduced, but still present, following intravenous hexamethonium administration (10 mg/kg). This residual enhancement was eliminated following subsequent administration of timolol (0.1 mg in 0.1 mL normal saline) into the ipsilateral stellate and middle cervical ganglia. Similar results were obtained when the order of administration of these agents was reversed. When the beta-adrenergic agonist isoproterenol (1, 2 or 5 micrograms in 1 microL of normal saline) was administered into specific loci of an acutely decentralized stellate or middle cervical ganglion, cardiac chronotropism and/or inotropism were increased; when similar injections were made into adjacent ganglionic sites cardiac responses usually were not elicited. Following hexamethonium administration similar results were obtained indicating that these effects were not primarily dependent upon nicotinic cholinergic synapses. In contrast, repeat injections of isoproterenol into the site that initiated cardiac responses when injected with isoproterenol failed to elicit any cardiac responses following local administration of timolol into the same site indicating that the effects of isoproterenol could be blocked by a beta-adrenergic receptor blocking agent. Injections of 1 to 5 micrograms of isoproterenol into a ganglion which was surgically disconnected from the heart failed to elicit cardiac responses, demonstrating that at these doses detectable activation of cardiac myocyte beta-adrenergic receptors via circulating isoproterenol which had leaked out of the ganglion did not occur. It is concluded that beta-adrenergic receptors in intrathoracic ganglia are involved in the efferent sympathetic regulation of the heart and that such receptors are associated with neurons in specific ganglionic loci.