Effects of calcium-free perfusion on excitation-contraction coupling in heart and skeletal muscle.

Interventricular septa and semimembranosus accessorius muscles (SMA) from the guinea pig and frog gastrocnemius (FG) muscles were vascularly perfused and isolated for mechanical and radioisotope flux measurements. Since calcium deprivation causes progressive electrical inexcitability, 100 muM La was included in all calcium-free solutions (0-Ca, 100-La) to stabilize the membrane. Perfusion of ventricular septa with such solutions resulted in tension (P) and dP/dt declines with half-times (t 1/2) = 11 sec, similar to the most rapid phase of 45Ca efflux. In contrast, the major component of tension decline during 0-Ca, 100-La perfusion of the SMA and FG muscles was much slower (t 1/2 =33 min). The rate of the slow component of 45Ca efflux from the SMA and FG muscles was essentially identical with the rate of the major tension decline. Significant tension (10-16 percent) was still present in these perfused skeletal muscles after 1-2 hr of 0-Ca, 100-La perfusion. Subsequent addition of La (200 muM total La) did not change the slope of P decline significantly for an additional 30-45 min. Addition of up to 2 mM EGTA after 30 min 0-Ca perfusion (calculated extracellular [Ca2+] less than 3x10(-9) M) altered but slightly the rate of P decline. These experiments emphasize the difference in the source of contractile Ca in heart and skeletal muscle and make it unlikely that there is a physiological "trigger" Ca for excitation-contraction (E-C) coupling in these muscles.