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Maximum relaxation was calculated and is expressed as a percentage of constriction in response to phenylephrine.
Maximum relaxation was calculated and expressed as a percentage of constriction to phenylephrine.
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A small but significant decrease in the maximum acetylcholine-induced relaxation was observed in angiotensin II-treated wild-type rings compared to saline control when comparing the entire curve but there was no change in EC50 (logEC50: −7.37 ± 0.08 vs. −7.46 ± 0.04 M, respectively, P = ns; n = 10) (Fig. 4e).
The magnitude of maximum relaxation, however, was not affected.
The maximum relaxation reached was 71±6%6% of the phenylephrine-induced vasoconstriction.
The percentage relaxation was recorded from the maximum contraction.
Acetylcholine-induced relaxation was attenuated by DEP (maximum relaxation reduced from 91±4%4% to 49 ± 6% with 100 μg/mL DEP; p < 0.001) but was restored by superoxide dismutase (SOD; maximum relaxation, 73 ± 6%; p < 0.001).
The amount of relaxation was reported as the percent of possible maximum relaxation achievable per ring, i.e., peak MCh response minus the resting tension.
The maximum contraction by 20 mM CaCl2 was taken as 100% contraction and percentage relaxation was calculated as a fraction of 100% contraction.
Myocardial relaxation was evaluated according to the left ventricular end-diastolic pressure (LVEDP) and the maximum descending rate of left ventricular pressure (−dP/dtmax) [ 11].
Endothelium-dependent relaxation was impaired in vessels of patients with CAD compared with those obtained from control subjects (maximum relaxation in response to A23187, 43±16 compared with 62±16%; P=0.001; Figures 1A and 1C).
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