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Endothelium
Journal of Endothelial Cell Research
Volume 6, 1998 - Issue 1
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Original Article

Mechanism of Increased Blood Flow by Estrogen

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Pages 81-82 | Published online: 13 Jul 2009

References

  • Collins P., Shay J., Jiang C., Moss J. Nitric oxide accounts tor dose-dependent estrogen-mediated coronary relaxation after acute estrogen withdrawal. Circulation 1994; 90: 1964–1968
  • Lamping K. G., Nuno D. W. effects of 17β-estradiol on coronary microvascular responses to endothelin-1. Am. J. Physiol 1996; 271: H1117–H1124
  • Moini H., Bilsel S., Bekdemir T., Emerk K. 17β-Estradiol increases intracellular free calcium concentration of human vascular endothelial cells and modulates its responses to acetylcholine. Endothelium 1997; 5: 11–19
  • Node K., Kitakaze M., Kosaka H., Minamino T., Sato H., Kuzuya T., Hori M. Roles of NO and Ca2+-Activated K+ channels in coronary vasodilation induced by 17β-estradiol in ischemic heart failure. Faseb J 1997; 11: 793–799
  • Van Buren G. A., Yang D., Clark K. E. Estrogen-induced uterine vasodilation is antagonized by L-nitro-arginine methyl ester, an inhibitor of nitric oxide synthesis. Am. J. Obstet. Gynecol 1992; 16: 828–833

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