Fig. 2.
Effect of blockade of the NO-cGMP pathway on PHE-induced contraction in pulmonary artery segments of normoxic, hypoxic, and MCT-treated rats. Pulmonary artery segments of normoxic (A and D), hypoxic (B and E), and MCT-treated rats (C and F) were either nontreated (○) or pretreated with the NOS inhibitor l-NAME (3 × 10−4 M) (●), or the guanylate cyclase inhibitor ODQ (10−5 M) (Δ) for 10 min. The tissues were stimulated with increasing concentrations of PHE, and the contractile response was measured and presented as grams per milligram tissue weight (A, B, and C) or as percentage of maximal PHE contraction (D, E, and F). Data represent means ± S.E.M. (n = 6–16). *, measurements in l-NAME- or ODQ-treated pulmonary artery segments are significantly different (p < 0.05) from corresponding measurements in nontreated segments.