Table 1.
Effects of various pharmacological inhibitors on vascular reactivity of Cmpd17b in the aorta.
| Agonist | Sample Size | Cmpd17b | |
| n | pEC50 | Rmax | |
| Control (DMSO) | 12 | 5.17 ± 0.06 | 69 ± 5 |
| L-NAME | 8 | 5.08 ± 0.04 | 72 ± 2 |
| Indo | 4 | 5.09 ± 0.15 | 74 ± 4 |
| Indo+L-NAME | 4 | 5.17 ± 0.10 | 67 ± 8 |
| Indo+L-NAME+KCaB | 4 | 5.27 ± 0.06 | 75 ± 8 |
| Endothelium intact | 6 | 5.07 ± 0.03 | 62 ± 5 |
| Endothelium denuded | 6 | 5.06 ± 0.03 | 55 ± 10 |
| Control (DMSO) | 6 | 5.09 ± 0.05 | 60 ± 2 |
| 50mM K+ | 4 | 5.13 ± 0.05 | 73 ± 8 |
| ODQ | 5 | 5.14 ± 0.09 | 71 ± 2 |
| Glibenclamide | 6 | 5.20 ± 0.18 | 52 ± 3 |
| Agonist | CaCl2 | ||
| n | pEC50 | Emax | |
| Control (DMSO) | 3 | 2.34 ± 0.23 | 111 ± 10 |
| Cmpd17b | 3 | ND | 0 * |
| Nifedipine | 3 | ND | 0 * |
Values are expressed as mean ± S.E.M; n, aorta from individual mice. DMSO, vehicle control; Rmax, maximum relaxation; Emax, maximum constriction relative to %KPSS; Indo, indomethacin; KCaB, combination of the small and intermediate conductance calcium-activated potassium channel inhibitors apamin and TRAM34; L-NAME, Nω-nitro-L-arginine methyl ester; ODQ, 1H-[1,2,4]oxadiazolo[4 ,3-a]quinoxalin-1-one; pEC50, sensitivity;. ND = not determined. * Significantly different from DMSO control (by one-way ANOVA, Dunnett’s post hoc test).