Table 1. Effects of compounds on porcine coronary artery relaxation response to G-1.
Compounds | % reduction of the G-1 relaxation | % relaxation | EC50 (μM) |
---|---|---|---|
G-1 + | 46.78 ± 2.52 (n = 10) | 0.027 | |
G-1 + BFA 50–100 μM | 44.90% | 25.78 ± 3.51 (n = 7) *** | 0.028 |
G-1 + BFA 100 μM + PKI 5 μM | 76.98% | 10.77 ± 0.87 (n = 11) *** | 0.174 |
G-1 + ESI-09 20 μM | 58.12% | 19.59 ± 3.73 (n = 4) *** | 0.146 |
G-1 + CE3F4 100 μM | 68.98% | 14.51 ± 3.35 (n = 4) *** | 0.028 |
DMSO ++ | 11.39 ± 5.31 (n = 6) | 5.56 | |
8CPT-2Me-cAMP (007) 90 μM +++ | 72.10 ± 13.55 (n = 6) **** | 49.4 | |
8CPT-2Me-cAMP (007) 90 μM + BFA 100 μM ++++ | 54.59 ± 4.22 (n = 4) *** | 49.5 |
Values are given as mean ± SEM. The number of experiments is indicated in parentheses.
***P<0.001
****P<0.0001, significant difference compared with control by using two-way ANOVA.
In rows 1–5 artery rings were pretreated with each of the inhibitors and the results were compared to G-1 (3 μM) alone group (+G-1).
In rows 6–8
++DMSO group was used as solvent control.
+++8-CPT-2Me-cAMP (007) was used as vasorelaxant agents and the result was compared to DMSO group.
++++Artery rings were pretreated with BFA, then relaxed with 8-CPT-2Me-cAMP (007) and the result was compared to 8-CPT-2Me-cAMP (007) alone group.