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. Author manuscript; available in PMC: 2010 Apr 28.
Published in final edited form as: Circulation. 2009 Apr 13;119(16):2161–2169. doi: 10.1161/CIRCULATIONAHA.108.815803

Figure 2. VSMC-selective PPARγ deletion increased responses to adrenergic receptor (AdR) agonists in aorta.

Figure 2

Figure 2

Figure 2

Phenylephrine (PE) (A) and norepinephrine (NE) (B) dose-dependent contraction curves of thoracic aorta rings from SMPG KO and LC mice. Results were shown as mean±S.E.M, n=12 in each group. *P < 0.05, **P < 0.01 versus LC, Bonferroni post-test. (C) Representative tracing of NE induced thoracic aorta response in SMPG KO mice. NE induced thoracic aorta relaxation (line b), and pre-incubation of aorta ring 10 min with 10−8 mol/L propanalol (line a) completely blocked the NE-induced relaxation effect. The dark circles indicate NE added into the incubation bath in a series of concentrations ranging from 10−11 to 10−6 mol/L (left to right). (D) Representative thoracic aorta ring tracing in response to β2-AdR agonist. Terbutaline (Terb) increased relaxation of the thoracic aorta ring in SMPG KO mice (line b) compared to LC mice (line a) originally pre-constricted by 10−7mol/L PE (indicated by an arrow). Dark circles indicate terbutaline added into the incubation bath in a series of concentrations ranging from 10−12 to 10−6 mol/L (left to right). (E): VSMC-selective PPARγ deletion did not affect thoracic aorta endothelium-dependent relaxation induced by acetylcholine (Ach) in aortic rings with intact endothelia, or (F) endothelium-independent relaxation induced by sodium nitroprusside (SNP) in aortic rings with the endothelium removed. Results are shown as mean±S.E.M, n=12 in each group.