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J Appl Physiol 85: 2040-2046, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 6, 2040-2046, December 1998

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

Michèle Sweeney, David Beddy, Valerie Honner, Bridget Sinnott, Ronan G. O'Regan, and Paul McLoughlin

Department of Human Anatomy and Physiology, University College, Dublin 2, Ireland

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 (Po)]. Endothelial removal did not alter this response. In aortic preparations, isohydric hypercapnia caused significant (P < 0.01) relaxation (-27.4 ± 3.2% Po), which was largely endothelium dependent. Normocapnic acidosis caused relaxation of PA (-20.2 ± 2.6% Po), which was less (P < 0.01) than that observed in aortic preparations (-35.7 ± 3.4% Po). Endothelial removal left the pulmonary response unchanged while increasing (P < 0.01) the aortic relaxation (-53.1 ± 4.4% Po). 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.

acidosis; vascular smooth muscle; nitric oxide; carbon dioxide


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