%0 Journal Article %1 Balk_1991_897 %A Balke, C. W. %A Wier, W. G. %D 1991 %J Circ. Res. %K 1742874 Acid, Animals, Buffers, Calcium, Concentration, Conductivity, Egtazic Electric Gov't, Guinea Myocardium, Non-U.S. Osmolar P.H.S., Pigs, Research Ryanodine, Sodium, Solutions, Support, U.S. %N 3 %P 897--902 %T Ryanodine does not affect calcium current in guinea pig ventricular myocytes in which Ca$^2+$ is buffered. %U http://circres.ahajournals.org/cgi/content/abstract/68/3/897 %V 68 %X Calcium current in mammalian ventricular muscle is altered in the presence of ryanodine. Previous studies performed on rat ventricular cells have shown a slowing of Ca$^2+$ current inactivation and suggest the hypothesis that ryanodine, by reducing the release of Ca$^2+$ from the sarcoplasmic reticulum, reduces the availability of Ca$^2+$ for inactivation of Ca$^2+$ current (Ca$^2+$-dependent inactivation). Another hypothesis is that the effects of ryanodine on Ca$^2+$ current are due to a mechanical connection of the ryanodine receptor with the L-type Ca$^2+$ channel. To further test these hypotheses we examined the effect of ryanodine on Ca$^2+$ current in single voltage-clamped guinea pig ventricular myocytes that contained Ca$^2+$ indicator and Ca$^2+$ buffer. We used fura 2 (pentapotassium salt) to confirm that the ryanodine we used was capable of abolishing Ca$^2+$ release from the sarcoplasmic reticulum during the period in which it was present. We perfused the cells with 10 mM EGTA to block changes in intracellular Ca$^2+$ concentration. In the absence of internal EGTA, Ca$^2+$ currents displayed biexponential inactivation and Ca$^2+$-dependent inactivation (steady-state inactivation curves turned up at positive potentials). Inactivation was slowed by ryanodine at 10 microM. In cells perfused internally with EGTA, however, ryanodine had no effects, and steady-state inactivation curves were not shifted to the right. We conclude that, in guinea pig ventricular myocytes, the effects of ryanodine on Ca$^2+$ current are mediated by Ca$^2+$ and thus the effects of ryanodine do not provide a basis on which to postulate a physical connection between the L-type Ca$^2+$ channel and the ryanodine receptor (sarcoplasmic reticulum Ca$^2+$ release channel).

@article{Balk_1991_897, abstract = {Calcium current in mammalian ventricular muscle is altered in the presence of ryanodine. Previous studies performed on rat ventricular cells have shown a slowing of {C}a$^{2+}$ current inactivation and suggest the hypothesis that ryanodine, by reducing the release of {C}a$^{2+}$ from the sarcoplasmic reticulum, reduces the availability of {C}a$^{2+}$ for inactivation of {C}a$^{2+}$ current ({C}a$^{2+}$-dependent inactivation). Another hypothesis is that the effects of ryanodine on {C}a$^{2+}$ current are due to a mechanical connection of the ryanodine receptor with the L-type {C}a$^{2+}$ channel. To further test these hypotheses we examined the effect of ryanodine on {C}a$^{2+}$ current in single voltage-clamped guinea pig ventricular myocytes that contained {C}a$^{2+}$ indicator and {C}a$^{2+}$ buffer. We used fura 2 (pentapotassium salt) to confirm that the ryanodine we used was capable of abolishing {C}a$^{2+}$ release from the sarcoplasmic reticulum during the period in which it was present. We perfused the cells with 10 mM EGTA to block changes in intracellular {C}a$^{2+}$ concentration. In the absence of internal EGTA, {C}a$^{2+}$ currents displayed biexponential inactivation and {C}a$^{2+}$-dependent inactivation (steady-state inactivation curves turned up at positive potentials). Inactivation was slowed by ryanodine at 10 microM. In cells perfused internally with EGTA, however, ryanodine had no effects, and steady-state inactivation curves were not shifted to the right. We conclude that, in guinea pig ventricular myocytes, the effects of ryanodine on {C}a$^{2+}$ current are mediated by {C}a$^{2+}$ and thus the effects of ryanodine do not provide a basis on which to postulate a physical connection between the L-type {C}a$^{2+}$ channel and the ryanodine receptor (sarcoplasmic reticulum {C}a$^{2+}$ release channel).}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Balke, C. W. and Wier, W. G.}, biburl = {https://www.bibsonomy.org/bibtex/28ff49e8b414fc29d8b2bb95f288f8e06/hake}, description = {The whole bibliography file I use.}, interhash = {c82b7d7a7b2cee1f05a7c905e7365677}, intrahash = {8ff49e8b414fc29d8b2bb95f288f8e06}, journal = {Circ. Res.}, keywords = {1742874 Acid, Animals, Buffers, Calcium, Concentration, Conductivity, Egtazic Electric Gov't, Guinea Myocardium, Non-U.S. Osmolar P.H.S., Pigs, Research Ryanodine, Sodium, Solutions, Support, U.S.}, month = Mar, number = 3, pages = {897--902}, pmid = {1742874}, timestamp = {2009-06-03T11:21:01.000+0200}, title = {Ryanodine does not affect calcium current in guinea pig ventricular myocytes in which {C}a$^{2+}$ is buffered.}, url = {http://circres.ahajournals.org/cgi/content/abstract/68/3/897}, volume = 68, year = 1991 }