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. Author manuscript; available in PMC: 2011 Nov 1.
Published in final edited form as: Steroids. 2010 Jan 7;75(11):788–793. doi: 10.1016/j.steroids.2009.12.007

Figure 1.

Figure 1

Estrogen contracts coronary arteries when NOS is uncoupled pharmacologically or by a disease state (diabetes). Isometric contractile force recordings demonstrate that 100nM 17β-estradiol (20 min), a known coronary vasodilator, contracts endothelium-denuded coronary arteries from normal pigs after treatment with 100μM N-monomethyl-L-arginine (LNMMA) to uncouple NOS activity (n=10; gray bars). Interestingly, estrogen produced the same level of contraction in untreated coronary arteries from diabetic pigs (n=5; black bars). Estrogen-induced contraction of these “diabetic” arteries was completely reversed by further addition of 1mM tempol, a superoxide dismutase mimetic.