Adenosine reduces the Ca2+ transients of isoproterenol-stimulated rat ventricular myocytes

Author:

Fenton R. A.1,Moore E. D.1,Fay F. S.1,Dobson J. G.1

Affiliation:

1. Department of Physiology, University of Massachusetts Medical School, Worcester 01655.

Abstract

Adenosine in the heart attenuates the contractile and metabolic effects of beta-adrenergic stimulation. The effect of adenosine on changes in intracellular Ca2+ concentration [( Ca2+]i) elicited with electrical stimulation was studied in rat ventricular myocytes in the absence and presence of isoproterenol (ISO). Fura-2 was utilized as a Ca2+ indicator. Autofluorescence was determined, and in vivo calibration was conducted, for each myocyte. Phenylisopropyladenosine (PIA; 10(-7) M; 5 min), an adenosine A1 receptor agonist, had no effect on the Ca2+ transient magnitude (TM) or the rate of Ca2+ transient decline determined at 150 nM Ca2+(i) (RD150). ISO (10(-8) M; 1 min) in the continued presence of PIA resulted in a 16% increase in the TM, but no change in the RD150. Inhibiting the PIA with 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 10(-7) M; 3 min) in the continued presence of ISO plus PIA resulted in a further 51% increase in the TM and a 57% increase in the RD150. In PIA-treated myocytes, ISO-induced spontaneous high-frequency Ca2+ transients occasionally were observed after the inhibition of PIA by DPCPX. The results of this study suggest that adenosine attenuates myocardial contractile responses to beta-adrenergic stimulation, in part, by reducing the beta-adrenergic-induced changes in the Ca2+ transients occurring in the contracting ventricular myocyte.

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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