H2S induces catecholamine secretion in rat adrenal chromaffin cells.

Hydrogen sulfide (H(2)S) is recognized as an important gaseous signaling molecule in mammalian tissues and exerts its modulating functions of different systems via targeting different ion channels and receptors. H(2)S can be synthesized from l-cysteine by cystathionine β-synthetase (CBS) or cystathionine γ-lyase (CSE). It has been reported recently that H(2)S can be synthesized and released in rat adrenal medulla chromaffin cells (AMCs) which play a critical role in the regulation of stress response by releasing catecholamine (CA). In the present study, we combined amperometry and whole-cell patch-clamp recording to explore the direct effect of exogenous H(2)S on CA release in AMCs and the underlying ionic mechanism. Amperometry showed that local application of NaHS, the H(2)S donor, evoked CA release from AMCs. Furthermore, the CA secretory response to NaHS was totally blocked by removing extracellular Ca(2+). Whole-cell patch-clamp experiments showed that H(2)S-induced CA release is produced by membrane depolarization generated by an inhibition of Ca(2+)-activated K(+) current [I(K(Ca)) current]. We conclude that H(2)S is capable of directly inducing CA release by inhibiting the I(K(Ca)) current. This conclusion indicates that H(2)S may involve in the response of adrenal medulla to stress by modulating I(K(Ca)) current and CA release in mammalian animals.