This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Patel, J. R. Articles by Moss, R. L. Search for Related Content PubMed PubMed Citation Articles by Patel, J. R. Articles by Moss, R. L.

(Circulation Research. 1995;77:943.)
© 1995 American Heart Association, Inc.

Articles

Cardiac Sarcoplasmic Reticulum Phosphorylation Increases Ca²⁺ Release Induced by Flash Photolysis of Nitr-5

Jitandrakumar R. Patel, Roberto Coronado, Richard L. Moss

From the Department of Physiology, University of Wisconsin Medical School, Madison.

Correspondence to Dr Richard L. Moss, Department of Physiology, University of Wisconsin Medical School, 1300 University Ave, Madison, WI 53706.

Abstract Effects on Ca²⁺-induced Ca²⁺ release due to phosphorylation of sarcoplasmic reticulum (SR) proteins were investigated in isoproterenol-treated saponin-permeabilized trabeculae from rat ventricles. In these experiments, Ca²⁺ release from the SR was induced by a rapid change in concentration of free Ca²⁺ (ie, trigger Ca²⁺) achieved by flash photolysis of nitr-5, and the amount of Ca²⁺ released was assessed by measuring isometric tension. Ca²⁺ uptake by the SR was more rapid, and the amount of Ca²⁺ released by a given concentration of trigger Ca²⁺ was greater in isoproterenol-treated trabeculae compared with control trabeculae. However, under the same conditions of Ca²⁺ loading, the amplitudes of caffeine-elicited tension transients in control trabeculae were similar to those in isoproterenol-treated trabeculae, suggesting that the Ca²⁺ available for release was similar in the two cases. Control experiments showed that there were no significant differences in Ca²⁺ sensitivity of tension between isoproterenol-treated and control trabeculae. Also, application of alkaline phosphatase to trabeculae that had previously been treated with isoproterenol returned SR Ca²⁺ release to control levels. We conclude that the greater release of Ca²⁺ in isoproterenol-treated trabeculae in response to a given concentration of trigger Ca²⁺ is due to phosphorylation of SR proteins, most likely the Ca²⁺ release channel.

Key Words: ventricular trabeculae • sarcoplasmic reticulum • Ca²⁺-induced Ca²⁺ release • flash photolysis • phosphorylation

This article has been cited by other articles:

				E. Carmeliet Cardiac Ionic Currents and Acute Ischemia: From Channels to Arrhythmias Physiol Rev, July 1, 1999; 79(3): 917 - 1017. [Abstract] [Full Text] [PDF]

				Y.-K. Ju and D. G Allen How does {beta}-adrenergic stimulation increase the heart rate? The role of intracellular Ca2+ release in amphibian pacemaker cells J. Physiol., May 1, 1999; 516(3): 793 - 804. [Abstract] [Full Text] [PDF]

				D.A Eisner, A.W Trafford, M.E Dnaz, C.L Overend, and S.C O'Neill The control of Ca release from the cardiac sarcoplasmic reticulum: regulation versus autoregulation Cardiovasc Res, June 1, 1998; 38(3): 589 - 604. [Abstract] [Full Text] [PDF]

				Y.G. Wang, J. Huser, L.A. Blatter, and S.L. Lipsius Withdrawal of Acetylcholine Elicits Ca2+-Induced Delayed Afterdepolarizations in Cat Atrial Myocytes Circulation, August 19, 1997; 96(4): 1275 - 1281. [Abstract] [Full Text]

				R. Zucchi and S. Ronca-Testoni The Sarcoplasmic Reticulum Ca2+ Channel/Ryanodine Receptor: Modulation by Endogenous Effectors, Drugs and Disease States Pharmacol. Rev., March 1, 1997; 49(1): 1 - 52. [Abstract] [Full Text] [PDF]

				L.-S. Song, S.-Q. Wang, R.-P. Xiao, H. Spurgeon, E. G. Lakatta, and H. Cheng {beta}-Adrenergic Stimulation Synchronizes Intracellular Ca2+ Release During Excitation-Contraction Coupling in Cardiac Myocytes Circ. Res., April 27, 2001; 88(8): 794 - 801. [Abstract] [Full Text] [PDF]