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Vol. 291, Issue 1, 44-52, October 1999
-Estradiol, Progesterone,
and Testosterone1
Department of Physiology and Biophysics and Center for Excellence
in Cardiovascular-Renal Research, University of Mississippi Medical
Center, Jackson, Mississippi
The clinical observation that coronary heart disease is more common in
men and postmenopausal women than in premenopausal women has suggested
cardiovascular protective effects of female sex hormones including
hormone-mediated coronary vasodilation. We investigated whether the sex
hormones induced coronary relaxation is due to a decrease in
[Ca2+]i as measured in single coronary smooth
muscle cells isolated from gonadectomized male and female pigs. In the
presence of external Ca2+, prostaglandin
F2
(PGF2;
10
5 M) and membrane depolarization by 51 mM KCl
caused significant cell contraction and maintained increase in
[Ca2+]i to 297 ± 4 and 341 ± 20 nM, respectively. At 109 to 6 × 107
M, 17
-estradiol, progesterone, and testosterone caused
inhibition of PGF2- and KCl-induced
contraction and [Ca2+]i with 17-estradiol
being most effective. 17
-Estradiol did not affect
PGF2-induced contraction, and the inhibition
of PGF2 contraction by 17-estradiol,
progesterone, or testosterone was abolished by tamoxifen and ICI
182,780, RU-486, or flutamide, respectively. 17-Estradiol caused
similar inhibition of PGF2- and KCl-induced
contraction and [Ca2+]i. Progesterone and
testosterone caused greater inhibition of PGF2-induced cell contraction and
[Ca2+]i compared with the KCl responses. In
Ca2+-free (2 mM EGTA) solution, caffeine (10 mM) and
carbachol (105 M), which activate Ca2+
release from intracellular stores, caused small cell contraction and
transiently increased [Ca2+]i to 256 ± 53 and 262 ± 32 nM, respectively. Sex hormones did not
significantly affect caffeine- or carbachol-induced contraction or
[Ca2+]i. Thus, 17-estradiol, progesterone,
and testosterone cause relaxation of coronary smooth muscle cells and
decrease [Ca2+]i mainly by inhibiting
Ca2+ entry from extracellular space but not
Ca2+ release from intracellular stores. The differences in
potency of sex hormones in reducing cell contraction and
[Ca2+]i suggest differences in the
sensitivity of the PGF2- and depolarization-activated Ca2+ entry pathways to inhibition
by sex hormones.
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