Inositol trisphosphate does not release Ca 2+ from permeabilized cardiac myocytes and sarcoplasmic reticulum

Abstract

The possibility that inositol 1,4,5-trisphosphate (IP 3) may act as a Ca +-mobilizing second messenger in cardiac muscle in a manner analogous to its actions in other cell types has been examined using saponin-per-meabilized myocytes and isolated cardiac sarcoplasmic reticulum. Myocytes permeabilized in the presence of MgATP 2+ sequestered Ca 2+ to a level of about 200 nM, similar to the cytosolic free Ca 2+ concentration of intact cells, but addition of Ip 3 was ineffective in causing Ca 2+ release from intracellular stores. Similarly, IP, (up to 50 μM) was unable to inhibit Ca 2+ uptake or cause Ca 2+ release from isolated canine cardiac sarcoplasmic reticulum vesicles in the presence of either EGTA or sodium vanadate. These results indicate that IP 3 is unlikely to mediate mobilization of intracellular Ca 2+ stores in myocardial cells. Co 2+ uptake Ca 2+ release Cardiac myocyte Sarcoplasmic reticulum Jnositol 1,4,5-trisphosphate