Fig. 5.
Effect of blockade of the NO-cGMP pathway on Phe-induced contraction in pulmonary artery of normoxic, hypoxic, and MCT-treated rats with or without treatment with NH4Cl (acidosis). Pulmonary artery rings of control normoxic (A), normoxic+acidosis (B), hypoxic (C), hypoxic+acidosis (D), MCT-treated (E), and MCT+acidosis rats (F) were either nontreated (○) or pretreated with the NO synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (l-NAME; 3 × 10−4 M; ●) or the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10−5 M; ▵) for 10 min. The tissues were stimulated with increasing concentrations of Phe, and the contractile response was measured and presented as g/mg tissue weight. Data represent means ± SE (n = 6–8). *Measurements in l-NAME-treated pulmonary artery segments are significantly different (P < 0.05) from corresponding measurements in nontreated segments. #Measurements in ODQ-treated pulmonary artery segments are significantly different (P < 0.05) from corresponding measurements in nontreated segments.