AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 274: H1308-H1314, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 4, H1308-H1314, April 1998

Do beta 2-adrenergic receptors modulate Ca2+ in adult rat ventricular myocytes?

Michael A. Laflamme and Peter L. Becker

Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322

We examined the role of beta 2-adrenergic receptors (ARs) in modulating calcium homeostasis in rat ventricular myocytes. Zinterol (10 µM), an agonist with a 25-fold greater affinity for beta 2-ARs over beta 1-ARs, modestly enhanced L-type calcium current (ICa) magnitude by ~30% and modestly accelerated the rate of Ca2+ concentration ([Ca2+]) decline (~35%) but had little effect on the magnitude of the [Ca2+] transient (a nonsignificant 6% increase). However, 1 µM of the highly selective beta 1-AR antagonist CGP-20712A completely blocked the ICa increase induced by 10 µM zinterol. Pretreatment of cells with pertussis toxin (PTX) did not alter ICa enhancement by 10 µM zinterol, although it did abolish the ability of acetylcholine to block the forskolin-induced enhancement of ICa. Zinterol (10 µM) approximately doubled adenosine 3',5'-cyclic monophosphate (cAMP) accumulation, although one-half of this increase was blocked by CGP-20712A. In contrast, 1 µM of the nonselective beta -agonist isoproterenol increased cAMP production 15-fold. Thus we found no evidence that activation of beta 2-ARs modulates calcium homeostasis in rat ventricular myocytes, even after treatment with PTX.

zinterol; CGP-20712A; calcium homeostasis; adenosine 3',5'-cyclic monophosphate


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