We examined mean (± S.E.M.) changes in wall tension in isolated rat intrapulmonary arteries on switching from control conditions (pH 7.38 ± 0.01; PCO2, 34.4 ± 0.5 mmHg) to hypercapnic acidosis (pH change, -0.24 ± 0.01; PCO2 change, +27.5 ± 0.9 mmHg), isohydric hypercapnia (pH change, -0.02 ± 0.01; PCO2 change, +28.5 ± 0.8 mmHg) and normocapnic acidosis (pH change, -0.24 ± 0.01; PCO2 change, -0.5 ± 0.3). Arteries were submaximally preconstricted with prostaglandin F2alpha; and changes in tension are expressed as a percentage of the 80 mM KCl-induced contraction (%Po). Mean changes in wall tension on switching to hypercapnic acidosis (+4.4 ± 3.7 %Po), isohydric hypercapnia (+1.9 ± 2.2 %Po) and normocapnic acidosis (-1.5 ± 1.9 %Po) were not significantly different from the change observed on switching to control conditions (+3.5 ± 1.1 %Po), and were unaltered by endothelial removal. In isolated carotid preparations, the change in tension in isohydric hypercapnia (-6.8 ± 7.1 %Po) was not significantly different from that observed in control switches (+8.6 ± 3.2 %Po). Significant reductions in tension (P < 0.001) were observed in hypercapnic (-42.9 ± 7.8 %Po) and normocapnic acidosis (-36.4 ± 9.0 %Po). These data suggest that intrapulmonary arteries are resistant to the vasodilator effects of extracellular acidosis observed in systemic (carotid) vessels.