Vol. 274, Issue 4, H1308-H1314, April 1998
Do 
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
2-adrenergic receptors (ARs) in
modulating calcium homeostasis in rat ventricular myocytes. Zinterol (10 µM), an agonist with a 25-fold greater affinity for
2-ARs over
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
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
-agonist isoproterenol increased cAMP production 15-fold. Thus we
found no evidence that activation of
2-ARs modulates calcium
homeostasis in rat ventricular myocytes, even after treatment with PTX.
zinterol; CGP-20712A; calcium homeostasis; adenosine
3',5'-cyclic monophosphate
