Table 4.
Teklad | Teklad→AIN | AIN | AIN→Teklad | |
---|---|---|---|---|
Emaxto [PE, 10−4.5M] and [KCl, 100 mM] | ||||
PE, %increase in force | 694.94 ± 34.53 (7) | 607.58 ± 51.55 (10) | 542.39 ± 49.85 (6) | 641.52 ± 62.37 (6) |
PE + l-NAME, %increase in force | 756.89 ± 61.56 (7) | 626.89 ± 61.39 (9) | 564.27 ± 57.82 (6) | 665.33 ± 79.91 (5) |
KCl, %increase in force | 312.35 ± 20.21(7) | 301.44 ± 27.24 (10) | 204.02 ± 27.88* (7) | 304.41 ± 50.57 (6) |
logEC50 | ||||
PE, M concn. | −5.9 ± 0.07 (7) | −5.9 ± 0.06 (10) | −5.9 ± 0.07 (6) | −5.9 ± 0.1 (6) |
PE + l-NAME, M concn. | −6.1 ± 0.02† (7) | −6.2 ± 0.09† (9) | −6.3 ± 0.1† (6) | −6.0 ± 0.08 (5) |
KCl, mM concn. | 52.4 ± 1.48 (7) | 50.2 ± 1.28 (10) | 49.5 ± 1.34 (7) | 47.9 ± 1.67 (6) |
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. l-NAME was used at 100-μM concentration to nonselectively inhibit NOS.
P < 0.05 for Emax vs. Teklad.
P < 0.05 vs. corresponding untreated mesenteric artery segment. Data were analyzed by two-way ANOVA.