CARDIAC SARCOPLASMIC-RETICULUM PHOSPHORYLATION INCREASES CA2-PHOTOLYSIS OF NITR-5( RELEASE INDUCED BY FLASH)

Effects on Ca2+-induced Ca2+ release due to phosphorylation of sarcopl asmic reticulum (SR) proteins were investigated in isoproterenol-treat ed saponin-permeabilized trabeculae from rat ventricles. In these expe riments, Ca2+ release from the SR was induced by a rapid change in con centration of free Ca2+ (ie, trigger Ca2+) achieved by flash photolysi s of nitr-5, and the amount of Ca2+ released was assessed by measuring isometric tension. Ca2+ uptake by the SR was more rapid, and the amou nt of Ca2+ released by a given concentration of trigger Ca2+ was great er in isoproterenol-treated trabeculae compared with control trabecula e. However, under the same conditions of Ca2+ loading, the amplitudes of caffeine-elicited tension transients in control trabeculae were sim ilar to those in isoproterenol-treated trabeculae, suggesting that the Ca2+ available for release was similar in the two cases. Control expe riments showed that there were no significant differences in Ca2+ sens itivity of tension between isoproterenol-treated and control trabecula e. Also, application of alkaline phosphatase to trabeculae that had pr eviously been treated with isoproterenol returned SR Ca2+ release to c entral levels. We conclude that the greater release of Ca2+ in isoprot erenol-treated trabeculae in response to a given concentration of trig ger Ca2+ is due to phosphorylation of SR proteins, most likely the Ca2 + release channel.