Electrophysiology of cardiac function in teleosts: cholinergically mediated inhibition and rebound excitation.

1. A study has been made on the responses of the plaice (Pleuronectes platessa) heart, isolated and in situ to differential vagal stimulation using intra- and extracellular recording electrodes. The effects of direct application of acetylcholine and catecholamines and their respective blocking agents are also reported.2. Vagal stimulation at 7 Hz totally inhibits heart beat whilst stimulation at 2-3 Hz accelerates it. Both these effects are blocked by atropine (10(-6) g/ml.). Bretylium (10(-5) g/ml.) and pronethalol (10(-6) g/ml.) have no effect upon either response to vagal stimulation.3. On cessation of prolonged inhibitory vagal stimulation there is a marked increase in the heart rate, and in quiescent hearts one or two beats are initiated after stimulation.4. Vagal stimulation gives rise to a hyperpolarization in atrial cells. It is proposed that all the excitatory effects of vagal stimulation are due to rebound excitation from an inhibitory hyperpolarization. At high frequencies the hyperpolarizations summate to give rise to total inhibition. At lower frequencies of stimulation the heart beat is increased to rates dependent on interaction between the time course of the hyperpolarization and the refractory period of the heart. Both effects are cholinergically mediated.5. The rebound excitation in response to vagal stimulation (post-vagal tachycardia) persists in response to stimulation of the atrial myocardium in the presence of atropine (10(-6) g/ml.) and bretylium (10(-5) g/ml.). It is therefore suggested that this is a response of the muscle cell membrane to vagal stimulation and is not nerve-mediated.