CHLORIDE-INDUCED CA2-RETICULUM OF CHEMICALLY SKINNED RABBIT PSOAS FIBERS AND ISOLATED VESICLES OF TERMINAL CISTERNAE( RELEASE FROM THE SARCOPLASMIC)

There is increasing evidence that Ca2+ release from sarcoplasmic retic ulum (SR) of mammalian skeletal muscle is regulated or modified by sev eral factors including ionic composition of the myoplasm. We have stud ied the effect of Cl- on the release of Ca2+ from the SR of rabbit ske letal muscle in both skinned psoas fibers and in isolated terminal cis ternae vesicles. Ca2+ release from the SR in skinned fibers was inferr ed from increases in isometric tension and the amount of release was a ssessed by integrating the area under each tension transient. Ca2+ rel ease from isolated SR was measured by rapid filtration of vesicles pas sively loaded with Ca-45(2+). Ca2+ release from SR was stimulated in b oth preparations by exposure to a solution containing 191 mM choline-C l, following pre-equilibration in Ca2+-loading solution that had propi onate as the major anion. Controls using saponin (50 mu g/ml), indicat ed that the release of Ca2+ was due to direct action of Cl- on the SR rather than via depolarization of T-tubules. Procaine (10 mM) totally blocked Cl-- and caffeine-elicited tension transients recorded using l oading and release solutions having ([Na+] + [K+]) x [Cl-] product of 6487.69 mM(2) and 12361.52 mM(2), respectively, and blocked 60% of Ca2 + release in isolated SR vesicles. Surprisingly, procaine had only a m inor effect on tension transients elicited by Cl- and caffeine togethe r. The data from both preparations suggests that Cl- induces a relativ ely small amount of Ca2+ release from the SR by activating receptors o ther than RYR-1. In addition, Cl- may increase the Ca2+ sensitivity of RYR-1, which would then allow the small initial release of Ca2+ to fa cilitate further release of Ca2+ from the SR by Ca2+-induced Ca2+ rele ase.