I(f) was shown to be present in adult human atrial and ventricular myocytes but data obtained from infant myocytes are lacking. We have studied I(f) in isolated ventricular myocytes from children undergoing surgical correction of tetralogy of Fallot (TOF; n = 5; mean age: 15.3 months). All recordings were made with the patch clamp technique in the whole cell mode at a temperature of 36-37 degrees C. A modified Tyrode solution containing 25 mM KCl was used to amplify I(f). Considering I(f) to be present when its current density at -120 mV was greater than 0.5 pA/pF, I(f) could be found in 28 out of 32 myocytes (88%). The mean current density was -2.01 +/- 0.3 pA/pF (mean +/- S.E.M.). First current activation occurred at -70 mV and I(f) could be reversibly inhibited by superfusing the myocytes with CsCl (2 mM). Half maximal activation (V(1/2)) of I(f) was at -80.3 +/- 1.0 mV (n = 28). Beta-adrenergic receptor stimulation with isoproterenol (1 microM) caused an acceleration of current activation and a shift of V(1/2) by 7.88 +/- 1.8 mV (n = 10) to less negative potentials. This study provides first evidence that the hyperpolarization-activated pacemaker current I(f) is present in infant human ventricular myocytes. Our results suggest that I(f) in ventricle of infants suffering from TOF has similar properties as I(f) in adult ventricle.