Table 2.
Teklad | Teklad→AIN | AIN | AIN→Teklad | |
---|---|---|---|---|
Emax to [ACh, 10−5.5 M] and [SNP, 10−6.5 M] | ||||
ACh, %PE | 99.71 ± 0.27 (6) | 99.53 ± 0.41 (10) | 100.24 ± 0.28 (6) | 100.14 ± 0.37 (6) |
ACh + l-NAME, %PE | 94.99 ± 0.39* (5) | 64.50 ± 15.34* (10) | 91.96 ± 2.76* (6) | 92.95 ± 1.46* (6) |
SNP, %PE | 97.36 ± 0.65 (7) | 96.65 ± 1.91 (10) | 98.24 ± 0.82 (7) | 98.54 ± 0.51 (6) |
logEC50 | ||||
ACh, M concn. | −7.1 ± 0.10 (6) | −7.4 ± 0.10 (10) | −7.2 ± 0.10 (6) | −7.2 ± 0.10 (6) |
ACh + l-NAME, M concn. | −6.2 ± 0.10* (5) | −6.3 ± 0.20* (8) | −6.6 ± 0.10* (6) | −6.7 ± 0.20 (5) |
SNP, M concn. | −7.9 ± 0.12 (7) | −8.0 ± 0.09 (10) | −7.9 ± 0.17 (6) | −8.4 ± 0.21 (5) |
Values are means ± SE; no. of rats are in parentheses. Dahl S rats were given Teklad or AIN standard chow diets at weaning (3 wk old). At 12 wk, weaning-diet groups were divided, and a subset of rats underwent a diet switch, generating two additional diet groups: Teklad→AIN and AIN→Teklad. Nω-nitro-l-arginine methyl ester (l-NAME) was used at 100-μM concentration to nonselectively inhibit nitric oxide synthase (NOS). ACh, acetylcholine; SNP, sodium nitroprusside; PE, phenylephrine. Brackets denote concentration.
P < 0.05 vs. corresponding untreated mesenteric artery segment. Data were analyzed by two-way ANOVA.