The quantal nature of calcium release to caffeine in single smooth muscle cells results from activation of the sarcoplasmic reticulum Ca(2+)-ATPase
Department of Physiology
Adenosine Triphosphate; Animals; Bufo marinus; Caffeine; Calcium; Calcium Channels; Calcium-Transporting ATPases; Cell Compartmentation; Cell Membrane Permeability; Cells, Cultured; Detergents; Dose-Response Relationship, Drug; Enzyme Activation; Enzyme Inhibitors; Ion Channel Gating; Muscle Proteins; Muscle, Smooth; Ryanodine Receptor Calcium Release Channel; Saponins; Sarcoplasmic Reticulum; Terpenes; Thapsigargin
Life Sciences | Medicine and Health Sciences
Calcium release from intracellular stores occurs in a graded manner in response to increasing concentrations of either inositol 1,4,5-trisphosphate or caffeine. To investigate the mechanism responsible for this quantal release phenomenon, [Ca2+] changes inside intracellular stores in isolated single smooth muscle cells were monitored with mag-fura 2. Following permeabilization with saponin or alpha-toxin the dye, loaded via its acetoxymethyl ester, was predominantly trapped in the sarcoplasmic reticulum (SR). Low caffeine concentrations in the absence of ATP induced only partial Ca2+ release; however, after inhibiting the calcium pump with thapsigargin the same stimulus released twice as much Ca2+. When the SR Ca(2+)-ATPase was rendered non-functional by depleting its "ATP pool," submaximal caffeine doses almost fully emptied the stores of Ca2+. We conclude that quantal release of Ca2+ in response to caffeine in these smooth muscle cells is largely due to the activity of the SR Ca(2+)-ATPase, which appears to return a portion of the released Ca2+ back to the SR, even in the absence of ATP. Apparently the SR Ca(2+)-ATPase is fueled by ATP, which is either compartmentalized or bound to the SR.
J Biol Chem. 1996 Jan 26;271(4):1821-4.
The Journal of biological chemistry
Steenbergen, Josef M. and Fay, Fredric S., "The quantal nature of calcium release to caffeine in single smooth muscle cells results from activation of the sarcoplasmic reticulum Ca(2+)-ATPase" (1996). Open Access Articles. 802.