Роль калиевых каналов в отрицательном инотропном эффекте сероводорода в предсердии мыши

The effect of sodium hydrosulfide (NaHS) donor of hydrogen sulfide (H 2S) on the force of contraction of isolated mouse atrium was studied. Cumulative application of NaHS in concentrations 100, 200 and 300 ^M induced dose-dependent decrease of the force of contraction, the maximum velocity of contraction and relaxation of the myocardium. A substrate of H 2S synthesis L-cysteine in concentrations 1, 10, 50 uM also had the negative inotropic action, whereas a blocker of H 2S synthesis p-cyano alanine caused an increase of the force of contraction. Inhibition of K-channels by tetraethylammonium (2 mM) caused the increase of the amplitude of contraction and the reduction of negative inotropic effect of NaHS in all used concentrations. After the inhibition of ATP-dependent K-channels by glibenclamide NaHS action was prevented in concentration 100 uM, significantly decreased in concentration 200 uM and didn't changed in concentration 300 uM. Activation of ATP-dependent K-channels by diazoxide did not affect the negative inotropic effect of NaHS. The obtained data suppose that in the mouse atrium exogenous and endogenous H 2S causes a reduction of the force of contraction, which is mediated by the activation of ATP-dependent, calcium-activated or voltage-dependent K-channels.