Regulation of atrial contraction in the seawater-adapted eel,Anguilla japonica

The atrium isolated from the seawater-adapted eel beats spontaneously in normal Ringer solution for more than 10 hr. The strength of beating was inhibited by acetylcholine (ACh) and the inhibitory effects were blocked by atropine, a muscarinic ACh-receptor antagonist, indicating existence of muscarinic ACh-receptor on the atrium. The atrial contractility was stimulated by catecholamines and their agonists; the order of potency being isoproterenol > adrenaline (AD) = noradrenaline (NA) > phenylephrine > clonidine. The stimulatory effects of AD was completely blocked by propranolol, a β-adrenoceptor antagonist, but not by phentolamine, an α-adrenoceptor antagonist. These data were consistent with characteristics of β-adrenoceptors. Further characterization of the β-receptor was not attempted. The positive inotropic and chronotropic actions of AD were not completely blocked either by atenolol, a β₁-adrenoceptor antagonist, or by ICI 118551, a β₂-adrenoceptor antagonist. When electrical current with a short duration (0.25 msec) was passed through the atrium, the beating was inhibited initially, then enhanced later. The initial inhibition was inhibited by atropine and the later enhancement was blocked by propranolol. These results indicate that the electrical stimulation releases ACh and catecholamine(s) from the nerve endings. The positive inotropic and chronotropic effects of catecholamines were mimicked by tyramine, a catecholamine releaser from sympathetic nerve endings.