Abstract

Both catecholamine (CA) released from adrenal chromaffin cells and hydrogen sulfide (H2S) have been shown to play critical roles in the regulation of hypoxic stress response. Our previous study has demonstrated that exogenous H2S directly induced quantal CA released from adult rat adrenal chromaffin cells (ARACCs) by inhibiting Ca2+-activated K+ current [IK(Ca) current]. However, it is not clear now whether H2S can also directly induce quantal CA released from neonatal rat adrenal chromaffin cells (NRACCs). In the present study, we investigated whether exogenous H2S can stimulate quantal CA released from NRACCs, and whether there were differences in the kinetics of H2S-induced quantal CA released between ARACCs and NRACCs. Using carbon-fiber amperometry and whole-cell patch clamping techniques, our experimental results showed: (1) H2S can directly induce quantal CA released from NRACCs; (2) H2S induced the depolarization of membrane potential and inhibited IK(Ca) current; (3) compared with ARACCs, much smaller quantal size and faster quantal release were showed in NRACCs through the kinetic analysis of the single-vesicle secretion induced by H2S. Our results may not only help to further understand the H2S-induced CA released from adrenal chromaffin cells in the aspect of development, but also provide the insights for the clinical prevention and therapy for hypoxic stress-induced injury in neonates at birth.

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