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Research ArticleArticle

Estrogen Alters Relative Contributions of Nitric Oxide and Cyclooxygenase Products to Endothelium-Dependent Vasodilation

Jennifer Case and Cathy A. Davison
Journal of Pharmacology and Experimental Therapeutics November 1999, 291 (2) 524-530;
Jennifer Case
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Cathy A. Davison
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Abstract

The purpose of this study was to determine the effects of in vivo estrogen manipulations on mechanisms of endothelium-dependent vasodilation. Ovary-intact, ovariectomized (OVX), or OVX with estrogen replacement (OVX + E2) female Sprague-Dawley rats were studied (n = 8). Mesenteric arteries (∼300 μm) were isolated, cannulated, and pressurized to 60 mm Hg in an arteriograph containing bicarbonate buffer and vessel diameter was monitored. Concentration-response curves to the endothelium-dependent histamine H1 agonist 2-thiazolylethylamine (2-TEA; 1 nM–100 μM) and to acetylcholine (1 nM–10 μM) were performed in preconstricted arteries. The effect ofNω-nitro-l-arginine (LNA; 100 μM) or LNA + indomethacin (INDO) (10 μM) on agonist-induced vasodilation was determined. There was no difference between treatment groups in the sensitivity of mesenteric arteries to 2-TEA or acetylcholine. LNA produced a significant decrease in sensitivity to 2-TEA in arteries from ovary-intact and OVX + E2 rats but not in those from OVX rats. The addition of INDO produced a small additional decrease in sensitivity to 2-TEA in arteries from ovary-intact rats, a significant decrease in OVX, and no shift in OVX + E2. LNA + INDO produced a similar degree of inhibition of the 2-TEA response in the three treatment groups. In contrast, when acetylcholine was used, the decrease in sensitivity produced by LNA or LNA + INDO was similar in the three rat groups. We conclude that estrogen increases the nitric oxide component of endothelium-dependent dilation and decreases the cyclooxygenase component. These effects of estrogen appear to be agonist-specific. Our findings suggest that estrogen modulates cross talk between the nitric oxide synthase and cyclooxygenase pathways of vasodilation.

Footnotes

  • Send reprint requests to: Cathy A. Davison, Ph.D., Department of Pharmacology and Neuroscience, Albany Medical College, 47 New Scotland Ave., Albany, NY 12208. E-mail:Cathy_Davison{at}ccgateway.amc.edu

  • ↵1 This work was supported by grants (to C.A.D.) from the National Institutes of Health (HL 45673) and from Albany Medical College.

  • Abbreviations:
    NO
    nitric oxide
    OVX
    ovariectomized
    E2
    estrogen
    PSS
    physiological salt solution
    2-TEA
    2-thiazolylethylamine
    LNA
    Nω-nitro-l-arginine
    INDO
    indomethacin
    SPERNO
    spermine-nitric oxide complex
    • Received March 10, 1999.
    • Accepted July 13, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 291 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 291, Issue 2
1 Nov 1999
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Research ArticleArticle

Estrogen Alters Relative Contributions of Nitric Oxide and Cyclooxygenase Products to Endothelium-Dependent Vasodilation

Jennifer Case and Cathy A. Davison
Journal of Pharmacology and Experimental Therapeutics November 1, 1999, 291 (2) 524-530;

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Research ArticleArticle

Estrogen Alters Relative Contributions of Nitric Oxide and Cyclooxygenase Products to Endothelium-Dependent Vasodilation

Jennifer Case and Cathy A. Davison
Journal of Pharmacology and Experimental Therapeutics November 1, 1999, 291 (2) 524-530;
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