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. 2005 Oct 3;146(7):972–982. doi: 10.1038/sj.bjp.0706398

Table 2.

NA, ET-1 and PdBu Rmax and pD2 values in mesenteric arteries from control and diabetic rats

  Control Diabetic
  Rmax pD2 Rmax pD2
  g –log EC50 g log EC50
Noradrenaline
 Untreated (13) 1.35±0.10 6.84±0.1 1.86±0.09* 7.13±0.13*
 Ro-318220 1.15±0.09 6.40±0.06** 1.44±0.09** 6.63±0.04**
 Untreated (8) 1.51±0.09 6.81±0.06 1.93±0.08* 7.11±0.08*
 Calphostin C 1.43±0.23 6.47±0.09** 1.16±0.09** 6.88±0.09*,**
         
Endothelin
 Untreated (4) 1.57±0.21 8.16±0.14 1.92±0.34 8.24±0.17
 Ro-318220 0.76±0.12** 7.97±0.08 0.67±0.16** 7.97±0.05
 Untreated (5) 1.66±0.11 8.43±0.19 1.94±0.20 8.27±0.11
 Calphostin C 0.82±0.19** 8.08±0.15 0.69±0.12** 8.07±0.18
         
Phorbol 12,13 dibutyrate
 Untreated (8) 2.13±0.27 7.28±0.09 1.97±0.29 7.32±0.11
 Ro-318,220 ND ND ND ND

Mesenteric arteries were isolated from control and diabetic rats and cumulative concentration response curves to NA, ET-1 and PdBu were constructed in the absence and presence of PKC inhibitors, Ro-318220, 3 μM for 30 min, and calphostin C, 3 μM for 30 min. Number in parentheses represents number of animals. ND, not detectable.

*

P<0.05 compared to corresponding control value,

**

P<0.05 compared to corresponding untreated value (two-way ANOVA followed by Newman–Keuls post hoc test).