| pubmed-article:3708768 | pubmed:abstractText | We have examined the effects of ryanodine, an inhibitor of the release of sarcoplasmic reticulum calcium in cardiac muscle, on contractile tension and calcium-45 movement in aortic smooth muscle of guinea pigs to learn whether this agent also modifies the release of stored calcium in vascular smooth muscle. Ryanodine (3-100 microM) suppressed the phasic contractions induced by caffeine and norepinephrine in calcium-free medium and prevented the stimulation of calcium-45 efflux by these agonists. Ryanodine did not significantly alter either the contractile response or the increased cellular influx of calcium-45 caused by high potassium in more than 1 mM calcium, suggesting that this agent does not affect depolarization-induced calcium entry into the cells. In a calcium-free, high potassium solution, the addition of calcium at concentrations of 1 mM and less resulted in a contraction which appeared to depend largely on the release of calcium from intracellular stores. This contraction was blocked by ryanodine. These data are consistent with the hypothesis that ryanodine causes a diminished release of calcium from the intracellular store in vascular smooth muscle, as it does in cardiac muscle. Moreover, our results indicate that a calcium-induced calcium release may exist in smooth muscle, and that this release is antagonized by ryanodine. | lld:pubmed |
