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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. 3.

Fig. 3

ER-mediated relaxation in cephalic, thoracic and abdominal arteries of female rat. Endothelium-intact segments of thoracic aorta (open circles), carotid (open triangles) and pulmonary artery (open squares) as well as abdominal aorta (closed circles), mesenteric (closed triangles) and renal artery (closed squares) were precontracted with submaximal concentration of Phe and the steady-state contraction was recorded. Increasing concentrations (10−12 to 10−5 M) of 17β-estradiol (E2, activator of most ERs) (A), PPT (ERα agonist) (B), DPN (ERβ agonist) (C), or G1 (GPR30 agonist) (D) were added and the % relaxation of Phe contraction was measured. Data represent means±SEM, n= 8 to 10. * Significantly different (p<0.05) from corresponding measurement in thoracic aorta [T], carotid [C], pulmonary [P], abdominal aorta [A], mesenteric [M] and renal artery [R].