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pubmed:abstractText |
Resistance pulmonary arteries constrict in response to hypoxia, whereas conduit pulmonary arteries typically do not respond or dilate slightly. One proposed mechanism for this differential response is the variable expression of pulmonary arterial smooth muscle cell voltage-gated K(+) (K(V)) channel subunits (Kv1.2, Kv2.1, Kv1.5, and Kv3.1b) shown to be O(2) sensitive in heterologous expression systems. In this study, immunoblotting and immunohistochemistry were used to examine the expression of K(V) channel alpha- and beta-subunits in the bovine pulmonary arterial circulation to determine whether differential K(V) channel subunit distribution is responsible for the distinct sensitivities of pulmonary arteries to hypoxia. Surprisingly, there was little difference in the expression levels of Kv1.2, Kv1.5, and Kv2.1 between conduit and resistance pulmonary arteries. In contrast, expression of the Kv3.1b alpha-subunit and Kv beta.1, Kv beta 1.2, and Kv beta 1.3 accessory subunits dramatically increased along the pulmonary arterial tree. The differential expression of all the beta-subunits but of only one of the putative O(2)-sensitive alpha-subunits suggests that the alpha-subunits alone are not the O(2) sensors but further implicates the auxiliary beta-subunits in pulmonary arterial O(2) sensing.
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