The influence of the redox state potential on heart activity was examined. It was established that (1) Increasing the redox state potential by redox agents, the pacemaker activity gradually begins to diminish. This diminution manifests itself primarily in amplitude of contractions. (2) Increasing the redox state potential, acetylcholine effects a positive and not a negative inotropic effect, in other words, the oxidants cause a complete inversion of the typical ACh action. (3) Decreasing the redox state potential, the negative inotropic effect is increased. (4) Following an oxidant pretreatment, the Na+ -Ca2+ input through electro-genie channels is decreased, but the K+ efflux is increased. (5) Reductant pretreatment results in an inverse effect. As the redox state potential of the heart tissue is by 60 mV lower than that of the skeletal muscles — in other words, more reducing in character—the presumed role of the actual redox state potential in evoking pacemaker activity and causing negative inotropic action of acetylcholine in heart is discussed.