Hypoxic pulmonary vasoconstriction is unchanged in nadph-oxidase "knock-out" mice

K. Weir, M. Dinauer, D. Nelson, S. Archer

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The enzyme, NADPH-oxidase, has been suggested as a possible oxygen sensor in both the pulmonary vasculature and the carotid body. To examine this possibility, the pressor response to hypoxia was recorded in the isolated, Krebsperfused, lungs from 9 transgenic mice in which NADPH-oxidase had been eliminated (TM) and in 9 "wild-type" controls (CTR). Lucigenin-enhanced (LCL) and unenhanced (CL) chemiluminescence from the surface of the lungs was measured as an indication of oxygen radical production. CL was less in TM (17 ± 1 counts/0.1 sec, mean ± SEM) compared to CTR (27 ± 5, p <.05). LCL was 13 ± 2 in TM and 329 ± 75 counts/0.1 sec in CTR (p < .005). However, the increase in perfusion pressure caused by hypoxia was the same : TM 2.2 ± 0.5 mmHg and CTR 2.9 ± 0.8 mmHg. We conclude that the absence of NADPHoxidase does not alter the pressor response to hypoxia in the mouse but does markedly reduce chemiluminescence from the lung surface. This enzyme is unlikely to be the oxygen sensor in the pulmonary vasculature.

Original languageEnglish (US)
Pages (from-to)A99
JournalFASEB Journal
Issue number3
StatePublished - 1996
Externally publishedYes


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