Table 4

Effects of PBZ (300 nM) treatment in the presence of 10, 30, and 100 nM prazosin on residual receptors (q) and KA(μM) on responses to PE in the DVS

EC50 ControlEC50TreatedEmax Control versus PBZ TreatedKAqn
μM μM μM
Vehicle1.98  ± 0.60.81  ± 0.144-a 131.5  ± 7.1  versus  132.5  ± 6.34-a 10
PBZ 300 nM1.58  ± 0.1951.35  ± 31.944-a 130.8  ± 3.7  versus  50.3  ± 15.54-150 51.93  ± 15.224-a 0.039  ± 0.024
+10 nM prazosin protection1.99  ± 0.1133.04  ± 7.844-a 4-150 144.3  ± 5.4  versus  115.4  ± 8.44-150 311.53  ± 183.794-a 0.127  ± 0.0311
2-h washout of 10 nM prazosin control1.72  ± 0.578.37  ± 2.944-a 5
+30 nM prazosin protection8.56  ± 2.0932.68  ± 18.794-a 130.1  ± 6.1  versus  97.9  ± 7.14-150 237.18  ± 196.604-a 0.343  ± 0.134
2-h washout of 30 nM prazosin control3.453.522

Emax values are expressed as a percentage of 100 mM K+ contraction. Values are mean ± S.E.M. (n).

  • Statistical comparisoms: as in Table 3.

  • One-way analysis of variance was used to compare KAvalues; none were significantly different (p > .05), but q values were significantly different (p < .05) with q from 10 nM prazosin significantly different than q from 30 nM prazosin protection.

  • 4-150  Significantly different from corresponding controls (p < .05).

  • 4-a Not significantly different from corresponding controls (p > .05).