Table 2.
Effect of various antagonists/interventions on capsaicin-induced relaxations in porcine isolated artery segments
| Antagonist or other intervention (n) | Emax (%) | Δ Emax | pEC50 | Δ pEC50 |
|---|---|---|---|---|
| Porcine distal coronary artery | ||||
| (Control) (56) | 96 ± 1 | 5.27 ± 0.09 | ||
| Olcegepant (1 μM) (10) | 92 ± 2 | 3 ± 2 | 5.26 ± 0.11 | −0.02 ± 0.11 |
| CGRP8–37 (10 μM) (5) | 97 ± 3 | −2 ± 5 | 4.78 ± 0.06 | 0.00 ± 0.03 |
| Capsazepine (5 μM) (7) | 99 ± 1 | −3 ± 2 | 5.15 ± 0.26 | 0.26 ± 0.16 |
| Ruthenium red (0.1 mm) (12) | 88 ± 3 | 7 ± 4 | 4.89 ± 0.09 | 0.47 ± 0.23 |
| L-733060 (5 μM) (7) | 88 ± 3 | 4 ± 4 | 4.89 ± 0.09 | −0.04 ± 0.15 |
| Denuded endothelium (9) | 91 ± 4 | 2 ± 2 | 5.62 ± 0.49 | 0.21 ± 0.16 |
| l-NAME (0.1 mM) (6) | 90 ± 8 | 8 ± 8 | 4.84 ± 0.15 | 0.28 ± 0.31 |
| (Control) (15) | 99 ± 0 | 5.08 ± 0.15 | ||
| 18-α-Glycyrrhetinic acid (10 μM) (3) | 99 ± 1 | 0 ± 1 | 5.73 ± 0.75 | −0.59 ± 0.53 |
| 4-Aminopyridine (1 mM) (7) | 96 ± 2 | 3 ± 2 | 4.84 ± 0.15 | −0.46 ± 0.35 |
| Charybdotoxin (0.5 μM) + apamin (0.1 μM) (11) | 99 ± 1 | 0 ± 1 | 5.27 ± 0.15 | −0.04 ± 0.20 |
| Y-276323 (1 μM) (9) | 96 ± 2 | 3 ± 2 | 5.17 ± 0.19 | 0.04 ± 0.21 |
| Y-276323 (1 μM) + 4-Aminopyridine (1 mM) (8) | 96 ± 3 | 4 ± 3 | 5.22 ± 0.20 | 0.00 ± 0.11 |
| Porcine proximal coronary artery | ||||
| (Control) (4) | 100 ± 0 | 5.33 ± 0.42 | ||
| Olcegepant (1 μM) (4) | 90 ± 6 | 5.79 ± 0.16 | ||
| Porcine basilar artery | ||||
| (Control) (3) | 97 ± 1 | 4.70 ± 0.05 | ||
| Olcegepant (1 μM) (3) | 100 ± 0 | 4.97 ± 0.24 | ||
| Capsazepine (5 μM) (3) | 100 ± 0 | 4.80 ± 0.01 | ||
| Porcine meningeal artery | ||||
| (Control) (3) | 99 ± 1 | 4.82 ± 0.02 | ||
| Olcegepant 1 μM (3) | 99 ± 1 | 4.88 ± 0.04 | ||
Emax is the maximum relaxant response, expressed as percentage of the respective precontraction; pEC50 is the −logEC50, where EC50 is the concentration of agonist required to produce half the maximal response. The arteries were precontracted with KCl (18–30 mM) except where KCl (45–90 mM; bold) or U46619 (ital).