Redox regulation of autorhythmic heart contractions and the effect of acetylcholine failed to manifest itself by decreasing [Ca2+]0.
Earlier it was described by us, that the amplitude and frequency of cyclic autorhythmic contraction of frog heart was decreased by oxidants but increased by reductants. Increasing the redox state potential, acetylcholine effects a positive and not a negative inotropic action. Decreasing the redox state potential, the negative inotropic effect is increased. In search of the site of action of these regulatory influences, the role of [Ca2+]0 was investigated recently and it was established, that: 1. Reducing the [Ca2+]0 by 50% and oxidation diminished the amplitude and frequency of cyclic autorhythmic contraction more expressively, than in normal saline. 2. The increase in cyclic rhythmicity caused by reductant failed to manifest itself in Ca2+ deficient Ringer. 3. The reversing action of oxidation on ACh effects was practically abolished following a decline in [Ca2+]0. 4. The effect of reductant to intensify the negative inotropic actions of acetylcholine suffered an inversion. Because both the redox regulation of quantitative and/or qualitative parameters of cyclic autorhythmic contractions and the ACh effect altered significantly and in a non-additive manner, following a decrement in [Ca2+]0, it seems to be clear, that as a site of action of redox regulation in normal saline, a change in the involvement of extracellular Ca2+ (presumably by altering its influx or absorbtive parameters) has to be taken into consideration.