Effects of ryanodine on cardiac subcellular membrane fractions.
Both the rate and the steady-state magnitude of net calcium accumulation by cardiac sarcoplasmic reticulum (SR) vesicles are increased by ryanodine. Sarcolemmal calcium transport mechanisms are not affected. The apparent augmentation of calcium accumulation by membrane vesicles from junctional SR derives not from an increase in the rate at which calcium is pumped into the vesicles, but from a slowing of the rate of calcium efflux. Recent results show that decamethonium blunts these effects of ryanodine, whereas valinomycin potentiates them. The mechanisms for these latter effects are not well understood, but may involve limitation and promotion, respectively, of access of potassium ion to the interior of the membrane vesicles.
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Besch
D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002451:Cell Compartmentation / Q000187:drug effects; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D011188:Potassium / Q000502:physiology; D012433:Ryanodine / Q000494:pharmacology*; D012508:Sarcolemma / Q000187:drug effects* / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects* / Q000378:metabolism
D000470:Alkaloids; D007473:Ion Channels; D012433:Ryanodine; D011188:Potassium; D002118:Calcium