[Relationship between the amplitude of myocardial contractions in frogs and the frequency of electrical stimulation. Role of external and intracellular calcium in the coupling of excitation and contraction].

Ionic currents were studied on the frog atrial trabeculae (Rana ridibunda) at 20 degrees C using a double sucrose gap voltage clamp arrangement. The net inward current peaks did not change in the course of repetitive stimulation (0,5/s) in contrast to the increase of the contraction amplitude (isometric tension) in the similar conditions (Bowdich staircase). The slow component of the net inward current revealed under the action of TTX (2-10(-8) g/ml) was increased upon the increase of external Ca concentration but was blocked when D-600 was introduced into the solution. The inhibitory action of D-600 on the contraction amplitude was frequency independent (in the ranges: 0,1--0,7/s). The decrease of external Na+ (isoosmotic replacement of 70% NaCl by sucrose) or the increase (5-fold) of the external Ca2+ significantly enhanced the myocardial contraction depressed with D-600. However these contractions fall in the course of rhythmical stimulation, and the effect being strongly dependent on the rate of stimulation. The results confirm the assumption (see: Biophysics, 6, 1024, 1976), that intracellular Ca stores (sarcoplasmic reticulum, internal surface of the cellular membrane) are involved in the control of the contractility in the amphibian myocardial cells. Many peculiarities of the excitation-contraction coupling in the frog myocardial cells can be explaned if one assumes that: 1) there is no space separation of primary uptake and release of Ca ion sites in the frog myocardium; 2) the system of "resting Ca chanels" in the frog myocardial cells is not so well developed as in the mammalian myocardial cells.