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Vol. 293, Issue 2, 592-598, May 2000
-Estradiol in Rat Hearts Treated with
Isoproterenol: Involvement of a Cyclic AMP-Dependent
Pathway1
Department of Physiology and Institute of Cardiovascular Sciences
and Medicine, Faculty of Medicine, The University of Hong Kong
(H.-Y.L., J.-S.B., T.M.W.); and Department of Pharmacology, Faculty of
Medicine, The Chinese University of Hong Kong (Y.W.K.), Hong Kong,
China
We determined the effects of 17
-estradiol, the most effective
estrogen, acutely administered, on the heart/ventricular myocyte with
or without treatment with isoproterenol (Iso). At 0.1 to 1 nM,
17-estradiol, which itself had no effect, reduced the heart rate and
developed pressures in the isolated perfused heart treated with
10
7 M Iso. One nanomolar 17-estradiol also inhibited
the cyclic AMP (cAMP) production in Iso-treated ventricular myocytes.
At 10 nM to 1 µM, 17-estradiol itself reduced the heart rate and incidence of ischemia/reperfusion-induced arrhythmias, with the exception of diastolic pressure. The effects of 17-estradiol on
heart rate, systolic and mean pressures, and arrhythmias were significantly enhanced in the heart/ventricular myocyte treated with
Iso. Tamoxifen, an estrogen receptor antagonist, did not antagonize the
effect of 17-estradiol on the Ca2+ current in
ventricular myocytes treated with Iso, nor did it alter the effect of
the hormone on the cAMP production augmented by Iso and forskolin. The
effects of 17-estradiol on Ca2+ current in the presence
or absence of tamoxifen and/or Iso were similar in male rats, which do
not possess the estrogen receptor, and female rats, which have the
estrogen receptor. In conclusion, we have shown for the first time that
estrogen at physiological concentrations modulates negatively the
stimulatory actions of Iso on the heart rate and cardiac contractility.
The effects may result from activation of an unknown membrane receptor
and the adenylate cyclase/cAMP pathway, which enhances Ca2+
influx across the L-type Ca2+ channel.
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