Fig. 5.
Chronic hypoxia (CH) augments endothelium-derived nitric oxide (EDNO)-dependent vasodilation to arginine vasopressin (AVP) without altering smooth muscle sensitivity to NO. A: total vasodilatory responses (percent reversal of U-46619-induced constriction) to AVP (25 nM) in lungs (in situ) from control and CH neonates. Experiments were conducted in the presence or absence of Nω-nitro-l-arginine (l-NNA; 300 μM). Values are means ± SE; n = 5–14/group (indicated in or below bars). *P < 0.05 vs. control; #P < 0.05 vs. vehicle, analyzed by two-way ANOVA followed by Student-Newman-Keuls post hoc comparison. B: total vasodilatory responses (percent reversal of U-46619-induced constriction) to spermine NONOate. Experiments were conducted in the presence of l-NNA to limit the contribution of endogenous NO production. Values are means ± SE; n = 5 for control and n = 5 for CH. Results were analyzed by two-way ANOVA.