Table 5.
Effects of extracellular K+ raising and of blockers of NO synthase, large-, intermediate-, small-conductance Ca2+-activated-, ATP-dependent-, and voltage-gated-K+ channels on relaxations evoked by 5′-N-ethylcarboxamidoadenosine (NECA, 0.1–300 μM) in the pig prostatic small arteries
| NECA | ||||
|---|---|---|---|---|
| N | It (mN) | pD2 | Emax (%) | |
| Control (on NA-induced contraction) | 6 | 5.4 ± 1.7 | 5.9 ± 0.1 | 100 ± 0 |
| Control (on KPSS-induced contraction) | 6 | 4.7 ± 1.7 | 5.2 ± 0.1* | 79.9 ± 4.8* |
| l-NOARG (100 μM) (on KPSS-induced contraction) | 6 | 4.8 ± 1.5 | 4.3 ± 0.1*,** | 65.4 ± 9.2* |
| On NA-induced contraction | ||||
| Control | 6 | 10.2 ± 2.1 | 5.3 ± 0.1 | 97.7 ± 1.7 |
| IbTX (100 nM) | 6 | 10.3 ± 3.1 | 5.2 ± 0.1 | 91.2 ± 5.1 |
| Control | 7 | 7.3 ± 1.5 | 5.6 ± 0.1 | 99.4 ± 0.3 |
| TRAM34 (20 nM) | 7 | 5.9 ± 1.3 | 5.0 ± 0.1* | 98.7 ± 0.8 |
| Control | 6 | 6.3 ± 1.3 | 5.2 ± 0.1 | 95.5 ± 2.3 |
| Apamin (0.5 μM) | 6 | 5.7 ± 1.9 | 4.7 ± 0.1* | 94.3 ± 2.7 |
| Control | 6 | 5.7 ± 0.7 | 5.7 ± 0.2 | 99.7 ± 0.3 |
| Glibenclamide (1 μM) | 6 | 4.9 ± 1.1 | 5.7 ± 0.2 | 100 ± 0 |
| Control | 6 | 7.2 ± 1.6 | 5.6 ± 0.2 | 98.6 ± 0.8 |
| 4-AP (1 mM) | 6 | 6.0 ± 1.2 | 5.7 ± 0.1 | 95.2 ± 1.1 |
Results are expressed as mean ± s.e.m. of n arteries. pD2 = −log EC50, where EC50 is the concentration of agonist producing 50% of the Emax
It initial tension, Emax is the maximal relaxation, expressed as a percentage of the 1 μM noradrenaline (NA)- or 60 mM KPSS-induced contraction
*,**P < 0.05 versus control and potassium-enriched (60 mM) saline solution (KPSS), respectively (paired t test for paired observations and analysis of variance and an a posteriori Bonferroni method for multiple comparisons)