Effects of ryanodine and 9,21-didehydroryanodine on caffeine-induced contraction of rat and guinea pig aortae.

  title={Effects of ryanodine and 9,21-didehydroryanodine on caffeine-induced contraction of rat and guinea pig aortae.},
  author={K M Ito and Takaaki Ikemoto and S Aoki and M Ota},
  journal={Japanese journal of pharmacology},
  volume={51 4},
We compared the effects of ryanodine and 9,21-didehydroryanodine (DH-ryanodine), which are present in commercial preparations of 'ryanodine', on the contractions of rat and guinea pig aortae induced by 20 mM caffeine and tested the dependence of the action of each substance on external Ca2+. With the first protocol, the aortae were incubated with ryanodine or DH-ryanodine for 20 min in Ca2(+)-containing medium, and caffeine was added at 2 min incubation in Ca2(+)-free medium. With the second… 
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Attenuated contractile response of diabetic rat aorta to caffeine but not to noradrenaline in Ca(2+)-free medium.
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Levamisole and ryanodine receptors. II: An electrophysiological study in Ascaris suum.
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Role of intracellular calcium stores in contrast medium-induced renal vasoconstriction.
The Ca2+ channel blockers partially inhibited contractions induced by contrast media, while KCl-induced contractions were completely abolished and Ionic and nonionic contrast media induced quantitatively different renal vasocontractions.
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Time- and use-dependent inhibition by ryanodine of caffeine-induced contraction of guinea-pig aortic smooth muscle.
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  • Chemistry, Medicine
    Biochemical and biophysical research communications
  • 1988
Ryanodine more potently inhibited the second or the subsequent contraction due to caffeine than the first one even after the agent was removed from the bath after first caffeine, suggesting that an opening of Ca2+ release channel enhances the interaction of ryanodine with the channel.
Ryanodine Inhibits the Release of Calcium from Intracellular Stores in Guinea Pig Aortic Smooth Muscle
The results indicate that a calcium-induced calcium release may exist in smooth muscle, and that this release is antagonized by ryanodine, consistent with the hypothesis that ryanODine causes a diminished release of calcium from the intracellular store in vascular smooth muscle.
Ryanodine activation and inhibition of the Ca2+ release channel of sarcoplasmic reticulum.
  • G. Meissner
  • Chemistry, Medicine
    The Journal of biological chemistry
  • 1986
The results suggested two possible modes of action of ryanodine: 1) a change in the gating mechanism of the channel which is not readily detected using the slowly permeating molecule L-glucose or 2) achange in channel structure which prevents its complete closing.
Ryanodine Alteration of the Contractile State of Rat Ventricular Myocardium: Comparison with Dog, Cat, and Rabbit Ventricular Tissues
  • J. Sutko
  • Biology, Medicine
    Circulation research
  • 1980
The results are consistent with ryanodine effecting a decreased availability of intracellular contractile Ca2+, perhaps through a diminishment of its release.
Ca2+-activated ryanodine binding: mechanisms of sensitivity and intensity modulation by Mg2+, caffeine, and adenine nucleotides.
The Ca2+-ryanodine receptor complex is a functional unit at the terminal cisternae (TC) of the sarcoplasmic reticulum (SR) whose proteins comprise the Ca2+ release channels which may be involved in
Structural aspects of ryanodine action and selectivity.
Ryanodol and didehydroryanodol have low toxicity to mice and little activity at the mammalian receptor, yet they are potent knockdown agents for injected houseflies or cockroaches, suggesting a possible difference in the target sites of mammals and insects.
The interaction of calcium and ryanodine with cardiac sarcoplasmic reticulum.
The data obtained support the hypothesis that ryanodine binding to the low-affinity site (Km about 17 microM) is responsible for closure of the calcium release channel and the subsequent increase in the calcium uptake rate of the sarcoplasmic reticulum.
Caffeine-induced contraction in vascular smooth muscle.
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The effects of ryanodine on passive calcium fluxes across sarcoplasmic reticulum membranes.
Ryanodine at concentrations of 0.01-10 microM increased, while greater concentrations of 10-300 microM decreased the calcium permeability of both rabbit fast twitch skeletal muscle junctional and canine cardiac sarcoplasmic reticulum membranes, indicating that the changes in membrane permeability caused by this agent can be determined in part by the experimental environment.
Isolation of the ryanodine receptor from cardiac sarcoplasmic reticulum and identity with the feet structures.
The present study suggests that basically similar machinery (the ryanodine receptor and foot structure) is involved in triggering Ca2+ release from cardiac and skeletal muscle SR, albeit there are distinct differences in the sensitivity to ryandine and other ligands in heart versus skeletal muscle.