The excitation-secretion coupling process requires Ca2+ influx through voltage-dependent Ca2+ channels (VDCC) but the contribution of L-type or N-type VDCC during the secretion from adrenal chromaffin cell is still on debate. In this study we explored the contribution of each VDCC to exocytosis in single rat adrenal chromaffin cells. Chromaffin cells were voltage-clamped clamped in the whole-cell recording mode. Ca2+ inward current (ICa) was elicited by depolarization from -70 mV to +10 mV and the change in cell membrane capacitance (Cm) was monitored as an indicator of the resultant exocytosis. The increase in Cm had positive correlation with the amount of ICa and replacing the internal Ca2+ buffer to high EGTA (5 mM) decreased the sensitivity of Cm increase to Ca2+ influx. After blockage of ICa with 100 microM Cd2+, there was no increase in Cm following membrane potential depolarization while INa was intact. To clarify the contribution of each type of VDCC to induce exocytosis during membrane potential depolarization, L- and N-type ICa were blocked selectively by Ca2+ channel antagonists. After blockage of L-type ICa with nicardipine (1 microM), ICa was blocked to 35 +/- 6.2% (mean +/- standard error) of control and the resultant change in Cm was reduced to 38 +/- 4.6% of control. Bay K-8644 (1 microM) enhanced ICa and the similar proportion of Cm was increased by this L-type VDCC agonist. On the other hand omega-conotoxin GVIA (1 microM), an N-type VDCC antagonist, blocked ICa to 60 +/- 4.3% of control and reduced the change in Cm to 58 +/- 3.9% of control.(ABSTRACT TRUNCATED AT 250 WORDS)