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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2013 Jul;62(1):26–40. doi: 10.1097/FJC.0b013e31828bc88a

Fig. 8.

Fig. 8

Contribution of NO, PGI2, and hyperpolarization factor to ERβ-mediated relaxation of cephalic, thoracic and abdominal arteries of female rat. Endothelium-intact segments of thoracic aorta (A), carotid (B) pulmonary (C) abdominal aorta (D), mesenteric (E) and renal artery (F) were either nontreated or pretreated for 15 min with L-NAME (3×10−4 M), L-NAME+indomethacin (INDO, 10−5 M), or L-NAME+INDO+TEA (30 mM). The vessels were precontracted with submaximal concentration of Phe then increasing concentrations (10−12 to 10−5 M) of DPN (ERβ agonist) were added and the % relaxation of Phe contraction was measured. The specificity of the relaxation effects of DPN were tested in blood vessels pretreated with the ERβ antagonist PHTPP (10−5 M). Data represent means±SEM, n= 8 to 10. * Maximal relaxation is significantly different (p<0.05) from corresponding measurements in control nontreated vessels. # Measurements in vessels treated with the ERβ antagonist PHTPP are significantly different (p<0.05) from corresponding measurements in control nontreated vessels.