Effects of changes in pH and CO₂ on pulmonary arterial wall tension are not endothelium dependent

We examined the changes in isolated pulmonary artery (PA) wall tension on switching from control conditions (pH 7.38 ± 0.01, PCO₂ 32.9 ± 0.4 Torr) to isohydric hypercapnia (pH change 0.00 ± 0.01, PCO₂ change 24.9 ± 1.1 Torr) or normocapnic acidosis (pH change -0.28 ± 0.01, PCO₂ change - 0.3 ± 0.04 Torr) and the role of the endothelium in these responses. In rat PA, submaximally contracted with phenylephrine, isohydric hypercapnia did not cause a significant change in mean (± SE) tension [3.0 ± 1.8% maximal phenylephrine-induced tension (P(o))]. Endothelial removal did not alter this response. In aortic preparations, isohydric hypercapnia caused significant (P < 0.01) relaxation (-27.4 ± 3.2% P(o)), which was largely endothelium dependent. Normocapnic acidosis caused relaxation of PA (-20.2 ± 2.6% P(o)), which was less (P < 0.01) than that observed in aortic preparations (-35.7 ± 3.4% P(o)). Endothelial removal left the pulmonary response unchanged while increasing (P < 0.01) the aortic relaxation (53.1 ± 4.4% P(o)). These data show that isohydric hypercapnia does not alter PA tone. Reduction of PA tone in normocapnic acidosis is endothelium independent and substantially less than that of systemic vessels.