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J Biol Chem, Vol. 274, Issue 2, 628-637, January 8, 1999

Evidence for a beta 2-Adrenergic/Arachidonic Acid Pathway in Ventricular Cardiomyocytes
REGULATION BY THE beta 1-ADRENERGIC/cAMP PATHWAY

Catherine Pavoine, Sandrine Magne, Anne Sauvadet, and Françoise Pecker

From INSERM Unité 99, Hôpital Henri Mondor, 94010 Créteil, France

The signaling pathway mediating the contractile effect of beta 2-adrenergic receptors (beta 2-AR) in the heart is still matter of debate. By using embryonic chick ventricular cardiomyocytes that express both functional beta 1-and beta 2-ARs, we show here that the specific beta 2-AR agonist, zinterol, increases the amplitude of Ca2+ transients and cell contraction of electrically stimulated cells. Zinterol, up to 10 µM, did not stimulate adenylyl cyclase activity, and its effect on Ca2+ transients was unmodified by the specific cAMP antagonist, (Rp)-cAMPS. In contrast, zinterol (10-100 nM) triggered arachidonic acid (AA) release from [3H]AA-loaded cells via the activation of the cytosolic phospholipase A2 (cPLA2). Stimulation of the Ca2+ transients by zinterol was abolished by the cPLA2 inhibitor, AACOCF3, and was mimicked by AA (0.3-3 µM). Both stimulations of [3H]AA release and of [Ca2+]i cycling by zinterol were abolished after treatment of the cardiomyocytes with pertussis toxin. Although cell responses to beta 2-AR stimulation were mediated by AA, they were under cAMP control as follows: (i) the beta 1-AR stimulation exerted a cAMP-mediated negative constraint on the beta 2-AR/cPLA2 pathway; (ii) cAMP potentiated AA action downstream beta -AR stimulation. We conclude that, in cardiomyocytes, beta 2-AR is coupled to cPLA2 activation via a pertussis toxin-sensitive G protein. These results demonstrate the involvement of the cPLA2/AA pathway in mediating positive inotropic effects, which could potentially compensate for a defective cAMP pathway.

Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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