Characterization of Ca2+ release from the sarcoplasmic reticulum of myocardium and vascular smooth muscle.
The effects of Ca2+ and inositol-1,4,5-trisphosphate (IP3) as putative inducers of Ca2+ release from sarcoplasmic reticulum (SR) vesicles were studied. Addition of Ca2+ (5-50 microM) or caffeine (5 mM) to calcium loaded SR vesicles from canine ventricular myocardium caused immediate release of Ca2+; whereas, no such Ca2+ release was observed in canine aortic SR vesicles. Fractionation of the cardiac SR by zonal centrifugation of calcium/oxalate-loaded SR vesicles showed that Ca2+-induced Ca2+ release was present in a caffeine-sensitive, ryanodine-sensitive, calsequestrin-enriched fraction, probably derived from the junctional SR. By contrast, IP3 (greater than 0.1 microM) stimulated Ca2+ release from aortic SR, but had no such effect on cardiac SR (even with 50 microM IP3. These data indicate a difference in Ca2+ release mechanisms in SR from the heart and vascular smooth muscle.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D004285:Dogs; D066298:In Vitro Techniques; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000494:pharmacology; D008861:Microsomes / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D007295:Inositol Phosphates; D002110:Caffeine; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium