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J Biol Chem, Vol. 274, Issue 2, 628-637, January 8, 1999
2-Adrenergic/Arachidonic Acid
Pathway in Ventricular Cardiomyocytes
1-ADRENERGIC/cAMP PATHWAY
From INSERM Unité 99, Hôpital Henri Mondor,
94010 Créteil, France
The signaling pathway mediating the contractile
effect of 2-adrenergic receptors
(2-AR) in the heart is still matter of debate. By using
embryonic chick ventricular cardiomyocytes that express both functional
1-and 2-ARs, we show here that the
specific 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 2-AR stimulation were
mediated by AA, they were under cAMP control as follows: (i) the
1-AR stimulation exerted a cAMP-mediated negative
constraint on the 2-AR/cPLA2 pathway; (ii)
cAMP potentiated AA action downstream -AR stimulation. We conclude
that, in cardiomyocytes, 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.
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