We hypothesized that pacing-induced congestive heart failure alters -adrenergic constriction in intrapulmonary bronchial arteries. Cumulative dose responses to norepinephrine (NE), phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) were determined in pressurized vessel segments. ED₅₀ values for NE and PE were higher for control (5.34 ± 0.09 and 4.27 ± 0.08 M, respectively) vs. paced (5.73 ± 0.10 and 5.06 ± 0.28 M, respectively) groups. Prazosin increased the ED₅₀ values for NE and PE in both control and paced groups. Yohimbine decreased NE ED₅₀ in the control group only. Endothelium removal or nitric oxide synthase (NOS) inhibition decreased control but not paced NE ED₅₀. Maximum vasodilation and sensitivity (i.e., ED₅₀ values) were decreased for ACh but were similar for SNP in paced vs. control groups. Secondary segments were more reactive than paired primary segments in both groups, although pacing effects on ED₅₀ were unrelated to branching order. In conclusion, adrenergic constriction of canine intrapulmonary bronchial arteries is predominantly mediated via ₁-adrenoreceptors and is enhanced after pacing. Endothelium-derived relaxing factor(s) normally opposes -adrenergic vasoconstriction but not after pacing in this vasculature.