Role of Ca2+ Channel in Development of Tension in Heart Muscle. Journal of Molecular and Cellular Cardiology (1987) 19, 527-553. In mammalian and amphibian hearts Ca2+ enters the myocardial cells via voltage-gated Ca2+ channels. The role of Ca2+ channels in transporting the activator Ca2+ was probed by examining the redevelopment of tension and ICa in voltage-clamped myocardial strips after step recovery of Ca2+ channel from photolabile Ca2+ antagonist. Comparison of the kinetics of redevelopment of tension in the frog and mammalian heart following the photoinactivation of Ca2+ channel blockers showed that in the frog heart tension redevelops fully in one beat, while 5 to 7 beats were required for full redevelopment of tension in the mammalian heart. Ca2+ depletion studies using Antipyrylazo III showed that extracellular Ca2+ depletion during the action potential occurs primarily via the Ca2+ channel. In the frog heart sufficient Ca2+ is transported from the extracellular space during a single beat to activate tension. In the mammalian heart ICa triggers the release of internal stores, which when only fully loaded caused full development of tension. ICa also was involved in loading the intracellular Ca2+ pools. Two types of Ca2+ channels have been identified in the mammalian myocytes. The low-threshold rapidly inactivating Ca2+ channels appear to be involved in trigger release of Ca2+, while the high threshold (conventional Ca2+ channels) seem to be involved primarily in reloading of internal Ca2+ pools.