Figure 3.
PGI2-, EDHF-, and NO-mediated endothelium-dependent relaxation in mesenteric arterial rings. Submaximal phenylephrine contraction (EC80) was elicited, acetylcholine (ACh) was added to arterial rings in presence of selective inhibitors as described in methods and Table 1, and then the percentage of relaxation to phenylephrine contraction was measured to determine (A) PGI2-, (B) EDHF-, and (C) NO-mediated mesenteric arterial relaxation. Data (mean±SEM) represent measurements from 14 to 24 vascular rings from 7–9 rats per treatment group. *P≤0.05 vs control.