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Am J Physiol Lung Cell Mol Physiol 280: L264-L271, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 2, L264-L271, February 2001

Ion exchange activity in pulmonary artery smooth muscle cells: the response to hypoxia

Jane A. Madden1,2, Daniel E. Ray3, Peter A. Keller2, and Jack G. Kleinman2,3

Departments of 1 Neurology and 3 Medicine, The Medical College of Wisconsin, Milwaukee 53226; and 2 Research Service, Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295

The purposes of this study were to determine 1) the presence of the major ion transport activities that regulate cytoplasmic pH (pHc) in cat pulmonary artery smooth muscle cells, i.e., Na+/H+ and the Na+-dependent and -independent Cl-/HCO3- exchange, 2) whether pHc changes in cells from small (SPAs) and large (LPAs) pulmonary arteries during hypoxia, and 3) whether changes in pHc are due to changes in the balance of exchange activities. Exchange activities as defined by physiological maneuvers rather than molecular identity were ascertained with fluorescence microscopy to document changes in the ratio of the pHc indicator 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein. Steady-state pHc was higher in LPA than in SPA normoxic smooth muscle cells. SPAs and LPAs possessed all three transport activities; in HCO3--containing normoxic solutions, Cl-/HCO3- exchange rather than Na+/H+ exchange set the level of pHc; in HCO3--containing hypoxic solutions, pHc increased in SPA and decreased in LPA cells; altering the baseline pHc of a cell type to that of the other did not change the direction of the pHc response during hypoxia. The absence of Na+ prevented hypoxia-induced alkalinization in SPA cells; in both cell types, inhibiting the Cl-/HCO3- exchange activities reversed the normal direction of pHc changes during hypoxia.

cat; sodium/hydrogen exchange; sodium-dependent chloride/bicarbonate exchange; sodium-independent chloride/bicarbonate exchange


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