Acute effects of 17β-estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs

M. P. Bracamonte, M. Jayachandran, K. S. Rud, V. M. Miller

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25 Scopus citations


Our experiments were designed to determine the acute effects of 17β-estradiol on femoral veins from intact and ovariectomized female pigs. Rings of femoral veins with or without endothelium were suspended in organ chambers for measurement of isometric force. Concentration-response curves to 17β-estradiol (10-9 to 10-5 M) were obtained in veins contracted with prostaglandin F in the absence and presence of inhibitors of either estrogen receptors (ICI-182780; 10-5 M), nitric oxide synthase [NG-monomethyl-L-arginine (L-NMMA); 10-4 M], soluble guanylate cyclase (1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 10-5 M), or potassium channels (tetraethylammonium; 10-2 M). Estrogen receptors were identified with the use of Western blotting and immunostaining in veins of both groups. 17β-Estradiol caused acute endothelium-dependent relaxations in both groups. Relaxations to 17β-estradiol were inhibited by L-NMMA and 1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-l-one but not ICI-182780. Tetraethylammonium inhibited relaxations only in veins with endothelium from intact females. Results indicate that 17β-estradiol causes acute endothelium-dependent relaxations in femoral veins. The relative contribution of nitric oxide and K+ channels as mechanisms involved in relaxations to 17β-estradiol in femoral veins is modulated by ovarian status.

Original languageEnglish (US)
Pages (from-to)H2389-H2396
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 52-6
StatePublished - Dec 1 2002


  • Endothelium
  • Hyperpolarizing factor
  • Nitric oxide
  • Potassium channels

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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