Electrophysiological and cyclic AMP responses to beta-adrenergic receptor stimulation and catecholamine levels in cat and rabbit sympathetic ganglion

Abstract

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) > salbutamol ⪢ tazolol. Beta-adrenergic antagonists inhibited the ISO response in the following order of potency: propranolol > exaprolol ⪢ 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 electrophysiological 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.