Effects of asymmetric dimethylarginine on renal arteries in portal hypertension and cirrhosis

Table 4 pD₂ and maximal response values for the concentration-response curves to acetylcholine in renal arteries from Sham, partial portal vein ligation, and bile duct ligation groups in the absence (Control) and in the presence of N^G-nitro-L-arginine methyl ester or asymmetric dimethylarginine

Acetylcholine	n	pD2	Emax (%)
Sham
Control	8	7.95 ± 0.08	93 ± 3
L-NAME (3 × 10-4 mol/L)	8	7.13 ± 0.28a	24 ± 7a
ADMA (3 × 10-4 mol/L)	8	7.27 ± 0.13ac	60 ± 3ac
PPVL
Control	8	7.92 ± 0.08	94 ± 2
L-NAME (3 × 10-4 mol/L)	8	7.24 ± 0.11a	21 ± 3a
ADMA (3 × 10-4 mol/L)	8	7.18 ± 0.15a	65 ± 6ac
BDL
Control	8	7.91 ± 0.10	95 ± 3
L-NAME (3 × 10-4 mol/L)	8	7.13 ± 0.35a	24 ± 8a
ADMA (3 × 10-4 mol/L)	8	7.17 ± 0.22a	32 ± 6ace

pD₂, - log M of acetylcholine causing 50% of the maximal relaxation; Emax, maximal relaxation expressed as a percentage of the contraction in response to 3 × 10^-6 mol/L norepinephrine; n = number of rats.

^aP < 0.05 vs control group,

^cP < 0.05 vs L-NAME treated group and

^eP < 0.05 vs Sham and PPVL groups with the same treatment. ADMA: Asymmetric dimethylarginine; L-NAME: N^G-nitro-L-arginine methyl ester.