Regulation of Ca2+ release from internal stores in cardiac and skeletal muscles

It is widely accepted that Ca2+ is released from the sarcoplasmic reticulum by a specialized type of calcium channel, i.e., ryanodine receptor, by the process of Ca2+-induced Ca2+ release. This process is triggered mainly by dihydropyridine receptors, i.e., L-type (long lasting) calcium channels, di rectly or indirectly interacting with ryanodine receptor. In addition, mult iple endogenous and exogenous compounds were found to modulate the activity of both types of calcium channels, ryanodine and dihydropyridine receptors . These compounds, by changing the Ca2+ transport activity of these channel s, are able to influence intracellular Ca2+ homeostasis. As a result not on ly the overall Ca2+ concentration becomes affected but also spatial distrib ution of this ion in the cell. In cardiac and skeletal muscles the release of Ca2+ from internal stores is triggered by the same transport proteins, a lthough by their specific isoforms. Concomitantly, heart and skeletal muscl e specific regulatory mechanisms are different.