title: Activation of Ca2+ release in isolated sarcoplasmic reticulum.
abstract: The relationship between Ca2+ release from sarcoplasmic reticulum, induced by elevated pH, tetraphenylboron (TPB-) or chemical modification, and the change in the surface charge of the membranes as measured by the fluorescence intensity of anilinonaphthalene sulfonate (ANS) is examined. The simulated Ca2+ release is inhibited by dicyclohexylcarbodiimide and external Ca2+. TPB-, but not tetraphenylarsonium (TPA+), causes a decrease in ANS- fluorescence, with 50% decrease occurring at about 5 microM TPB-. The decrease in ANS- fluorescence as well as the inhibition of Ca2+ accumulation induced by TPB- are prevented by TPA+. A linear relationship between the decrease in membrane surface potential and the extent of the Ca2+ released by TPB- is obtained. Similar levels of [3H]TPB-bound to sarcoplasmic reticulum membranes were obtained regardless of whether or not the vesicles have taken up Ca2+. The inhibition of Ca2+ accumulation and the [3H]TPB- incorporation into the membranes were correlated. Ca2+ release from sarcoplasmic reticulum, by pH elevation, chemical modification or by addition of NaSCN (0.2 to 0.5 M) or the Ca2+ ionophore ionomycin, is also accompanied by a decrease in ANS- fluorescence intensity. However, chemical modification and elevated pH affects the surface potential much less than SCN- or TPB- do. These results suggest that the enhancement of Ca2+ release by these treatments is not due to a general effect on the membrane surface potential, but rather through the modification of a specific protein. They also suggest that membrane surface charges might play an important role in the control mechanism of Ca2+ release.
authors.affiliation: Department of Biology, Ben Gurion University of the Negev, Beer Sheva, Israel.
authors.forename: V
authors.initials: V
authors.lastname: Shoshan-Barmatz
mesh_terms: D000817:Anilino Naphthalenesulfonates; D000818:Animals; D001152:Arsenicals / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D007425:Intracellular Membranes / Q000187:drug effects / Q000502:physiology; D007476:Ionophores / Q000494:pharmacology; D009132:Muscles / Q000648:ultrastructure; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology; D013050:Spectrometry, Fluorescence; D013499:Surface Properties; D013775:Tetraphenylborate / Q000494:pharmacology
chemical_list: D000817:Anilino Naphthalenesulfonates; D001152:Arsenicals; D015220:Calcium Channels; D007476:Ionophores; C009439:tetraphenylarsonium; D013775:Tetraphenylborate; D012965:Sodium Chloride; D002118:Calcium