Table 4 Emax and log EC50 values of vasomotor responses to acetylcholine (ACh), phenylephrine (Phe), DEA-NO and U46619 in mesenteric resistance arteries from sham-operated (SO) and microsurgical liver cholestasis (LC) rats.

From: Acute-on-chronic liver disease enhances phenylephrine-induced endothelial nitric oxide release in rat mesenteric resistance arteries through enhanced PKA, PI3K/AKT and cGMP signalling pathways

 

SO

LC

Emax (%)

log EC50

Emax (%)

log EC50

ACh

89.28 ± 5.9

−7.25 ± 0.21

91.57 ± 6.4

−7.32 ± 0.19

Phe + E

117.8 ± 2.3

−5.79 ± 0.03

112.9 ± 7.2

−5.52 ± 0.09*

Phe –E

123.1 ± 2.1

−6.01 ± 0.03#

124.6 ± 3.3

−5.93 ± 0.04#

Phe + E + L-NAME

118.2 ± 5.4

−6.25 ± 0.13+

130.8 ± 7.3

−5.83 ± 0.10+

DEA-NO

91.09 ± 2.9

−6.45 ± 0.09

93.78 ± 3.2

−7.28 ± 0.13*

DEA-NO + Tempol

94.41 ± 2.9

−6.57 ± 0.08

91.99 ± 1.9

−7.55 ± 0.07*

U46619

111.2 ± 4.2

−8.01 ± 0.07

103.7 ± 5.0

−7.34 ± 0.08*

  1. Results are expressed as means + S.E.M. n = 5–10 segments from different animals in each group. *P < 0.05 SO vs. LC. #P < 0.05 arteries with endothelium vs. arteries without endothelium. + P < 0.05 arteries without L-NAME vs. arteries incubated with L-NAME.
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