Table 2.
Effect of APO and PEG-SOD on −logEC50 and Emax of mouse thoracic aorta relaxation in response to ACh and SNP
| Control |
MSEW |
|||
|---|---|---|---|---|
| Agonist/Treatment | −logEC50 | Emax | −logEC50 | Emax |
| ACh | ||||
| VEH | 6.99 ± 0.12 | 73.2 ± 4.3 | 6.86 ± 0.07 | 53.5 ± 6.9* |
| APO | 7.27 ± 0.11 | 87.0 ± 5.8 | 7.31 ± 0.09† | 95.0 ± 2.1††† |
| PEG-SOD | 7.20 ± 0.10 | 81.5 ± 4.3 | 7.14 ± 0.12 | 77.3 ± 4.7† |
| SNP | ||||
| VEH | 8.54 ± 0.13 | 101.8 ± 0.7 | 8.23 ± 0.11 | 101.5 ± 0.7 |
| APO | 8.48 ± 0.18 | 102.9 ± 1.1 | 8.17 ± 0.11 | 100.4 ± 0.7 |
| PEG-SOD | 8.41 ± 0.14 | 102.3 ± 0.7 | 8.30 ± 0.09 | 100.4 ± 0.5 |
Values are means ± SE. Sensitivity (−logEC50) and maximal effect (Emax) values determined from %relaxation from phenylephrine preconstriction in response to agonist. Two-way ANOVA with Bonferroni post hoc analyses were performed for each agonist group [acetylcholine (ACh) or sodium nitroprusside (SNP)] with factors of group (Control, MSEW) and treatment [vehicle (VEH), apocynin (APO) or VEH, superoxide dismutase (PEG-SOD)]; n = 5–7 mice/group.
*
P < 0.05 compared with VEH Control;
†
P < 0.05, ††P < 0.01, and
†††
P < 0.001 compared with VEH MSEW.