Table 2.
Action of KCa1.1 channel inhibitors on K+ secretion
| IbTx |
Paxilline |
|||||
|---|---|---|---|---|---|---|
| IbTxΔΔIsc, μA/cm2 | IbTxΔΔIsc/secΔIsc | n | paxΔΔIsc, μA/cm2 | paxΔΔIsc/secΔIsc | n | |
| Basal | +9.9 ± 0.6* (0.0001) | −0.258 ± 0.033* (0.001) | 5 | +4.1 ± 1.2* (0.017) | −0.145 ± 0.059* (0.043) | 8 |
| Epinephrine | +20.8 ± 5.1* (0.027) | −0.281 ± 0.047* (0.010) | 5 | +16.4 ± 5.0* (0.013) | −0.216 ± 0.054* (0.005) | 8 |
| ATP(transient) | +11.6 ± 2.6* (0.047) | −0.654 ± 0.209 (0.089) | 3 | +9.6 ± 1.4* (0.002) | −0.454 ± 0.038* (0.0003) | 5 |
| ATP(sustained) | +3.1 ± 0.9 (0.074) | −0.293 ± 0.069* (0.052) | 3 | +3.9 ± 1.9 (0.104) | −0.317 ± 0.102* (0.036) | 5 |
Values are means ± SE (P values). Secretagogue-activated short-circuit current (secΔIsc = secretagogue − control) was measured for epinephrine (Fig. 1) and ATP (Fig. 3), and inhibitor-induced differences in secΔIsc (inhibΔΔIsc = inhibitor − control) were compared as well as the fractional inhibition (inhibΔΔIsc/secΔIsc). Inhibitors were added prior to secretagogue activation: paxilline (mucosal and serosal) 1.0 μM; IbTx (mucosal) 300 nM for basal and epinephrine, 200 nM for ATP. Significant differences from zero are indicated by asterisks (P values).