Temperature and nucleotide dependence of calcium release by myo-inositol 1,4,5-trisphosphate in cultured vascular smooth muscle cells.
Inositol 1,4,5-trisphosphate (IP3) rapidly increased 45Ca2+ efflux from a nonmitochondrial organelle in cultured vascular smooth muscle cells that were permeabilized with saponin. A nucleotide, preferably ATP, was essential for IP3-evoked 45Ca2+ release. Two nonhydrolyzable ATP analogues satisfied the nucleotide requirement for IP3-evoked 45Ca2+ release. IP3 strongly stimulated 45Ca2+ efflux at low temperatures (1 to 15 degrees C). Decreasing the temperature from 37 to 4 degrees C inhibited the rate of IP3-stimulated efflux by only about 33%. The failure of such low temperatures to strongly inhibit IP3-induced 45Ca2+ efflux suggests that IP3 activated a Ca2+ channel, rather than a carrier, by a ligand-binding, rather than a metabolic, reaction.
D000227:Adenine Nucleotides / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D002132:Calcium Radioisotopes; D002478:Cells, Cultured; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000494:pharmacology*; D007700:Kinetics; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D013329:Structure-Activity Relationship; D013403:Sugar Phosphates / Q000494:pharmacology*; D013696:Temperature; D013816:Thermodynamics
D000227:Adenine Nucleotides; D002132:Calcium Radioisotopes; D007295:Inositol Phosphates; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium