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Research ArticleArticle

Decreased [Ca2+]i during Inhibition of Coronary Smooth Muscle Contraction by 17β-Estradiol, Progesterone, and Testosterone

Jason G. Murphy and Raouf A. Khalil
Journal of Pharmacology and Experimental Therapeutics October 1999, 291 (1) 44-52;
Jason G. Murphy
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Raouf A. Khalil
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Abstract

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 F2α (PGF2α; 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 10−9 to 6 × 10−7M, 17β-estradiol, progesterone, and testosterone caused inhibition of PGF2α- and KCl-induced contraction and [Ca2+]i with 17β-estradiol being most effective. 17α-Estradiol did not affect PGF2α-induced contraction, and the inhibition of PGF2α contraction by 17β-estradiol, progesterone, or testosterone was abolished by tamoxifen and ICI 182,780, RU-486, or flutamide, respectively. 17β-Estradiol caused similar inhibition of PGF2α- and KCl-induced contraction and [Ca2+]i. Progesterone and testosterone caused greater inhibition of PGF2α-induced cell contraction and [Ca2+]i compared with the KCl responses. In Ca2+-free (2 mM EGTA) solution, caffeine (10 mM) and carbachol (10−5 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, 17β-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 PGF2α- and depolarization-activated Ca2+ entry pathways to inhibition by sex hormones.

Footnotes

  • Send reprint requests to: Raouf A. Khalil, M.D., Ph.D., Department of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216. E-mail:rkhalil{at}physiology.umsmed.edu

  • ↵1 This work was supported by grants from the American Health Assistance Foundation, the American Heart Association, Mississippi Affiliate (grant-in-aid), and National Institutes of Health Grants HL52696 and HL51971.

  • Abbreviations:
    CHD
    coronary heart disease
    PGF2α
    prostaglandin F2α
    IP3
    inositol-1,4,5-triphosphate
    • Received January 12, 1999.
    • Accepted June 14, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 291 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 291, Issue 1
1 Oct 1999
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Research ArticleArticle

Decreased [Ca2+]i during Inhibition of Coronary Smooth Muscle Contraction by 17β-Estradiol, Progesterone, and Testosterone

Jason G. Murphy and Raouf A. Khalil
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 44-52;

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Research ArticleArticle

Decreased [Ca2+]i during Inhibition of Coronary Smooth Muscle Contraction by 17β-Estradiol, Progesterone, and Testosterone

Jason G. Murphy and Raouf A. Khalil
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 44-52;
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