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(Circulation Research. 1996;79:147-151.)
© 1996 American Heart Association, Inc.

Articles

Cyclic ADP-Ribose Does Not Regulate Sarcoplasmic Reticulum Ca²⁺ Release in Intact Cardiac Myocytes

Xiaoqing Guo, Michael A. Laflamme, Peter L. Becker

the Department of Physiology, Emory University School of Medicine, Atlanta, Ga.

Correspondence to Dr Peter L. Becker, Department of Physiology, Emory University School of Medicine, 1648 Pierce Dr, Atlanta, GA 30322. E-mail plb@physio.emory.edu.

Cyclic ADP-ribose (cADPR), an intracellular second messenger known to mobilize Ca²⁺ in sea urchin eggs, has been implicated in modulating Ca²⁺ release in a variety of mammalian tissues. On the basis of studies of isolated cardiac sarcoplasmic reticulum (SR) vesicles and single SR Ca²⁺ release channels, cADPR has also been proposed to be a modulator of SR Ca²⁺ release in heart. In the present study, we directly examined the ability of cADPR to trigger SR Ca²⁺ release and to modulate Ca²⁺-induced Ca²⁺ release (CICR) in intact rat ventricular myocytes. Voltage-clamped myocytes were dialyzed with up to 100 µmol/L caged cADPR and 0.6 µmol/L calmodulin along with the Ca²⁺-sensitive dye fluo 3. A step increase in the cADPR concentration induced by flash photolysis of caged cADPR neither directly triggered SR Ca²⁺ release nor modulated CICR in intact myocytes. In contrast, under similar conditions, extracellular application of caffeine (1 to 2.5 mmol/L) onto myocytes produced both effects. Under equivalent conditions, flash photolysis of caged cADPR-loaded sea urchin eggs resulted in large Ca²⁺ transients. Further, the sustained presence of high cytosolic concentrations of either cADPR or its antagonist, 8-amino-cADPR, was ineffective in altering normal CICR in myocytes. These findings indicate that cADPR does not regulate SR Ca²⁺ release in intact cardiac myocytes.

Key Words: ventricular myocyte • cyclic ADP-ribose • Ca²⁺-induced Ca²⁺ release

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