Interplay Between Hydrogen Sulfide and Adrenergic and Muscarinic Receptors in the Mouse Atrium

Hydrogen sulfide (H 2 S) is synthesized endogenously, and it has a negative inotropic effect on myocardium of different animal species. Interaction between H 2 S and adrenergic and muscarinic receptors in regulation of mouse atrium contractile function was investigated in this study. Sodium hydrosulfide (NaHS, 300 μM), the H 2 S donor, decreased the contraction force of atrium. NaHS did not affect the positive inotropic effect of β-adrenoceptors (β-AR) activation by isoproterenol (ISO, 1 μM). The effect of the H 2 S donor under β-AR stimulation showed no differences comparison to control values. The agonist of muscarinic receptors carbachol (1 μM) induced a negative inotropic effect and partially prevented the reduction of cardiac muscle contractility by NaHS. Moreover, the effect of carbachol was more pronounced after preliminary application of NaHS. At the same time, after inhibition of β-AR (propranolol, 1 μM) or muscarinic receptors (atropine, 1 μM), negative inotropic effect of NaHS was the same as in control conditions. These results suggest that the H 2 S effects are mediated by intracellular signaling pathways activated by muscarinic receptors.