Estradiol relaxes rat aorta via endothelium-dependent and -independent mechanisms

Gamal Abou-Mohamed, Ahmed Elmarakby, Gerald O. Carrier, John D. Catravas, Robert W. Caldwell, Richard E. White

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

The effects of estrogen on arterial function are heterogeneous with respect to vessel and/or species. We have investigated 17β-estradiol-induced relaxation in isolated rat aorta with regard to the role of the vascular endothelium and ionic mechanisms. Estrogen induced a concentration-dependent relaxation of 46.5 ± 7.9% and 70.1 ± 12.2% (10-8 and 10-7 M), which was reduced by endothelial denudation. Furthermore, L-nitroarginine methyl ester completely abrogated this effect; however, estradiol did not relax KCl-contracted rings. Tetraethyl ammonium (1 mmol/l) completely blocked estradiol-induced relaxation. Estradiol increased [cGMP] in isolated aortic rings via NO, but did not significantly affect NOS activity in endothelial cells. Thus, estrogen can relax rat aorta in vitro via both endothelium-dependent and -independent mechanisms involving the NO/cGMP and potassium channel signaling system.

Original languageEnglish (US)
Pages (from-to)20-26
Number of pages7
JournalPharmacology
Volume69
Issue number1
DOIs
StatePublished - Aug 11 2003

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Keywords

  • Aorta
  • Estrogen
  • Nitric oxide
  • Potassium channel

ASJC Scopus subject areas

  • Pharmacology

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