Table 4.

Emax and −logEC₅₀ in thoracic aorta with PVAT intact (+PVAT) or without PVAT

	Flox	Flox + PVAT	HBK	HBK + PVAT
ACh-induced relaxation, % of PE
Emax	74.9 ± 6.0	91.8 ± 1.4†	87.0 ± 2.5	88.6 ± 3.9
−logEC50	−6.88 ± 0.10	−6.51 ± 0.13	−7.09 ± 0.11	−6.41 ± 0.06*
SNP-induced relaxation, % of PE
Emax	102.5 ± 1.1	101.8 ± 1.2	101.2 ± 0.6	102.4 ± 1.6
−logEC50	−7.52 ± 0.10	−6.52 ± 0.18†	−7.49 ± 0.08	−6.35 ± 0.08*
PE-induced constriction, % of KCl
Emax	92.8 ± 6.9	81.5 ± 5.7	77.6 ± 4.6	71.2 ± 4.1
−logEC50	−6.68 ± 0.07	−6.31 ± 0.09†	−6.57 ± 0.05	−6.14 ± 0.07*
AUC	191.5 ± 19.6	143.0 ± 15.1	153.2 ± 11.2	116.8 ± 10.4
KCl-induced constriction, % increase in force
Emax	122.5 ± 5.6	143.0 ± 6.6	121.0 ± 8.6	144.4 ± 3.5*
−logEC50	−6.07 ± 0.09	−6.60 ± 0.15†	−5.95 ± 0.07	−6.50 ± 0.08*
AUC	258.8 ± 18.2	364.8 ± 30.3†	243.1 ± 22.1	351.6 ± 17.6*

Values are presented as means ± SE; n = 6–10. Two-way ANOVA was used to compare effects of PVAT and genotype with Tukey’s post hoc test for cumulative concentration–response curves to assess vasorelaxation and vasoconstriction (Fig. 3). symbols indicate statistically significant differences (P < 0.05) for post hoc tests showing differences within genotypes with (+) and without (−)PVAT. AUC, area under the curve; HBK, hepatocyte-specific Bmal1 knockout; ACh, acetylcholine; PE, phenylephrine; PVAT, perivascular adipose tissue; SNP, sodium nitroprusside.

†P < 0.05 flox + PVAT vs. flox.

*P < 0.05 HBK + PVAT vs. HBK.