Hydrogen sulfide opens the KATP channel on rat atrial and ventricular myocytes.

Objective: Hydrogen sulfide (H(2)S), an endogenous gaseous transmitter, was found to protect the heart from various forms of injury, but the underlying mechanism is not known. H(2)S can open the K(ATP) channel on vascular smooth muscle cells, and the objective of this study was to determine whether H(2)S can open the K(ATP) channel on myocardiocytes.

Methods: The whole-cell patch-clamp technique was used to record I(K,ATP) and action potentials of atrial and ventricular myocytes isolated from the hearts of male Wistar rats. Sodium hydrogen sulfide (NaHS) was used as a donor of H(2)S to observe the effect of exogenous H(2)S on I(K,ATP). DL-propargylglycine (PPG), an inhibitor of the synthesis of H(2)S, was used at a concentration of 200 microM to observe the effect of endogenous H(2)S on I(K,ATP).

Results: NaHS at concentrations (in microM) of 9.375, 18.75, 37.5, 75 and 150 increased I(K,ATP) by 12.8% (p > 0.05), 28.4% (p < 0.05), 38.8% (p < 0.01), 51.2% (p < 0.01) and 58.6% (p< 0.01) on ventricular myocytes, respectively, and by 6.8% (p > 0.05), 10.4% (p > 0.05), 18.9% (p < 0.01), 24.8% (p < 0.01) and 37.2% (p < 0.01) on atrial myocytes, respectively. The H(2)S-induced decrease in the duration of action potentials (APD(90)) of ventricular myocytes was concentration-dependent, although only NaHS at a concentration of 150 microM decreased the APD(90) significantly (15%, p < 0.05). The H(2)S-induced decrease in APD(90) on atrial myocytes was concentration dependent, but the statistical difference was not significant. Inhibition of I(K,ATP) by PPG was time dependent and the level of inhibition was: ventricular myocytes, 7% (p > 0.05), 10% (p < 0.05), 15.3% (p < 0.01), 24.0% (p < 0.01) and 28.9% (p < 0.01); atrial myocytes, 15.8% (p > 0.05), 21.3% (p > 0.05), 26.5% (p < 0.01), 34.0% (p < 0.01) and 43.2% (p < 0.01) measured at 5, 10, 15, 20 and 25 min, respectively. The increase in the APD(90), by PPG was time dependent for ventricular myocytes [increased by 12.8% (p < 0.05) at 25 min]. The same was true for atrial myocytes, although only the value at 25 min was significant (15%, p < 0.05).

Conclusions: H(2)S decreased the APD(90),and both the endogenous and exogenous H(2)S-induced increase in I(K,ATP) on both atrial and ventricular myocytes was concentration dependent. These results may help to explain, at least in part, how H(2)S protects heart cells from various forms of injury.