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Estradiol relaxes rat aorta via endothelium-dependent and -independent mechanisms
  • G. Abou-Mohamed
  • A. Elmorakby
  • G. O. Carrier
  • J. D. Catraval
  • R. W. Caldwell
  • Richard E. White, Philadelphia College of Osteopathic Medicine
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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. Copyright © 2003 S. Karger AG, Basel.

This article was published in Pharmacology, Volume 69, Issue 1, Pages 20-26.

The published version is available at

Copyright © 2003 Karger.

Citation Information
G. Abou-Mohamed, A. Elmorakby, G. O. Carrier, J. D. Catraval, et al.. "Estradiol relaxes rat aorta via endothelium-dependent and -independent mechanisms" Pharmacology Vol. 69 Iss. 1 (2003) p. 20 - 26
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