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1 Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand Medical School, Johannesburg 2193, South Africa; and 2 Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655-0127
Adenosine
A2a receptor
(A2aR) stimulation enhances the
shortening of ventricular myocytes. Whether the
A2aR-mediated increase in myocyte
contractility is associated with alterations in the amplitude of
intracellular Ca2+ transients was
investigated in isolated, contracting rat ventricular myocytes using
the Ca2+-sensitive fluorescent dye
fura 2-AM. In the presence of intact inhibitory G protein pathways,
10
4 M
2-p-(2-carboxyethyl)phenethyl-amino-5'-N-ethylcarboxamidoadenosine (CGS-21680), an A2aR agonist,
insignificantly increased Ca2+
transients by 8 ± 5%, whereas myocyte shortening increased by 54 ± 1%. In contrast, 2 × 107 M isoproterenol, a
-adrenergic receptor agonist, increased
Ca2+ transients by 104 ± 15%
and increased myocyte shortening by 61 ± 6%. When
A2aR were stimulated in myocytes
that had the antiadrenergic actions of adenosine (Ado) abolished by
either treatment with pertussis toxin (PTx) or the presence of
8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine
A1-receptor antagonist, the
maximum increases in Ca2+
transients were similarly nominal (with PTx:
104 M CGS-21680, 14 ± 6% and 104 M Ado, 15 ± 4%; without PTx: 105 M Ado + 2 × 107 M DPCPX, 19 ± 1%). These results indicate that compared with -adrenergic
stimulation, which markedly increases myocyte
Ca2+ transients and shortening,
A2aR-mediated increases in myocyte shortening are accompanied by only modest increases in
Ca2+ transients. These
observations suggest that the
A2aR-induced contractile effects
are mediated predominantly by
Ca2+-independent inotropic mechanisms.
inotropic responses; adenosine receptors; intracellular calcium transients
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