Contraction and sarcoplasmic reticulum Ca²⁺ content in single myocytes of guinea pig heart: Effect of ryanodine

The relationship between the ability of sarcoplasmic reticulum (SR) to accumulate and retain Ca²⁺ and the electrically stimulated contractions (ESCs) of isolated cells from guinea pig ventricular myocardium was investigated. Caffeine contractures or rapid cooling contractures were used as a relative measure of the SR Ca²⁺ content. Depletion of SR Ca²⁺ by short exposure to caffeine (15 mM) or by prolonged rest resulted in a reduction of the amplitude of the ESCs by 83 ± 14 and 65 ± 11% (means ± SD), respectively. This result points to SR as a major source of the Ca²⁺ that activates contraction. However, depriving the SR of the ability to retain Ca²⁺ by means of prolonged (up to 75 min) exposure to 0.1 μM ryanodine (as shown by the absence of contractile response to caffeine or cooling) did not prevent an ESC of nearly normal amplitude (81 ± 24% control), albeit with a reduction contraction velocity and a time to peak contraction prolonged by 51 ± 11%. Additionally, while rest decay of ESCs was present after ryanodine treatment, the time for the ESCs to recover their steady-state amplitude was prolonged at least twofold. Thus, in contrast with the normal guinea pig cells, ESCs of the myocytes exposed to ryanodine are controlled by sarcolemmal processes. This change in the state of excitation-contraction coupling results mainly in modification of the time course of the ESCs and of the time course of the response of the cells to the change in the rate of stimulation.