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Effects of changes in pH and CO 2 on pulmonary arterial wall tension are not endothelium dependent

1998; American Physiological Society; Volume: 85; Issue: 6 Linguagem: Inglês

10.1152/jappl.1998.85.6.2040

8750-7587

Michèle Sweeney, D Beddy, Valerie Honner, Bridget Sinnott, Ronan G. O’Regan, Paul McLoughlin,

Respiratory Support and Mechanisms

We examined the changes in isolated pulmonary artery (PA) wall tension on switching from control conditions (pH 7.38 ± 0.01,[Formula: see text] 32.9 ± 0.4 Torr) to isohydric hypercapnia (pH change 0.00 ± 0.01,[Formula: see text] change 24.9 ± 1.1 Torr) or normocapnic acidosis (pH change −0.28 ± 0.01,[Formula: see text] 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.