Perivascular Adipose Tissue Inhibits Endothelial Function of Rat Aortas via Caveolin-1
Figure 2
The association between endothelium, endothelial vasodilators and perivascular adipose tissue (PVAT).
Original traces demonstrate contractile responses to incremental concentrations of phenylephrine (PE) (1 nM∼10 µM) in the presence and absence of PVAT (A).Statistical analysis of the PE-induced vasocontraction in the presence and absence of PVAT (n = 8) (B). Control experiment was shown as both original trace (C) and statistical analysis (n = 13) (D) of three times repeated contractile response to incremental concentrations of PE (1 nM∼10 µM). After endothelium denuded (-E) (E) or pretreatment of aorta with Nω-nitro-L-arginine methyl ester (L-NAME, 100 µM) (G), the original traces demonstrate contractile responses to incremental concentrations of PE (1 nM∼10 µM) in the presence and absence of PVAT. -E (n = 5) (F) or pretreatment of aorta with L-NAME (100 µM, n = 7) (H), concentration-response curves to PE was examined in the presence and absence of PVAT. Original traces demonstrate dilator response to incremental concentrations of acetylcholine (ACh) (1 nM∼10 µM) (I) or sodium nitroprusside (SNP) (0.1 nM∼1 µM) (K) in the presence and absence of PVAT. Vasodilator responses to ACh (n = 24) (J) and SNP (n = 5) (L) were performed in aortas in the presence and absence of PVAT. Values are means ± SEM for the numbers of animals in parentheses. *P<0.05 by two-way ANOVA compared with (−) PVAT of same treatment group. KCl, potassium chloride; (−) PVAT, absence of PVAT; (+) PVAT, presence of PVAT; 1st, PE-induced vasocontraction at the first time; 2nd, PE-induced vasocontraction at the second time; 3rd, PE-induced vasocontraction at the third time.