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The pacemaker current (I(f)) in embryonic chick ventricular myocytes is present, but decreases during development. beta-Adrenergic agonists stimulate I(f), whereas muscarinic cholinergic agonists inhibit I(f) and reverse beta-adrenoceptor stimulation. G-proteins directly and indirectly couple autonomic receptors to I(f) channels in embryonic ventricular cells. The I(f) may contribute partly to the electrogenesis of the pacemaker potential. On the other hand, Ito current, voltage-dependent and 4-AP-sensitive, exists even in young embryonic cardiomyocytes, but not in all cells. The Ito increases during development, resulting in modulation of the action potential configuration. The action potential duration of guinea pig ventricular myocardium decreases during the late fetal period and increases postnatally. Single cell voltage clamp analyses revealed that the decrease and increase in action potential duration are due to developmental increases in the current densities of the calcium current and delayed rectifier potassium current, respectively. The role of the sarcoplasmic reticulum in contraction and relaxation of the guinea pig myocardium increases during fetal development.

Developmental changes in the pacemaker current and membrane currents of the guinea pig myocardium.