Failure of Ba2+ and Cs+ to block the effects of vagal nerve stimulation in sinoatrial node cells of the guinea-pig heart

The aim of the study was to evaluate which ionic currents are modified in the sinoatrial node of guinea pigs when the vagus is stimulated. Responses of isolated atrial preparations to bilateral vagus nerve stimulation were examined. In bath-mounted preparations, 10-s trains of vagal stimulation (1–50 Hz) slowed the rate at which atrial contractions occurred. After the trains of stimuli, the force generated by each contraction was reduced. Both vago-inhibitory responses persisted in the presence of caesium (2 mM) and barium ions (1 mM). Vagal stimulation evoked a similar bradycardia in superperfused preparations in which intracellular recordings were made from pacemaker cells in the sinoatrial node. When pacemaking activity was abolished by adding the organic calcium channel antagonist nifedipine (1 μM) to the perfusate, vagal stimulation generated an inhibitory junction potential (IJP). Both the bradycardia and the amplitude of the inhibitory junction potential increased as the frequency of vagal stimulation was increased. The ability of vagal stimulation to produce inhibitory junction potentials was unaffected by the addition of caesium and barium ions to the perfusate. These observations suggest that the negative chronotropic and inotropic responses to vagal stimulation only minimally involve a muscarinically activated potassium current (IKACh) or changes in the hyperpolarization-activated pacemaker current Ih.