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Articles in PresS, published online ahead of print July 5, 2002
J Appl Physiol, 10.1152/jap.00564.2001
Submitted on June 4, 2001
Accepted on June 21, 2002
1 Medical Service, Department of Veteran's Affairs Medical Center, Salt Lake City, UT, USA; Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA
2 Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA
3 Department of Physiology, University of Utah School of Medicine, Salt Lake City, UT, USA
4 Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA; Medical Service, Department of Veteran's Affairs Medical Center, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: john.hoidal{at}hsc.utah.edu.
A current hypothesis proposes that oxygen (O2) sensing in type I cells of the carotid body and erythropoietin (epo) producing cells of the kidney involves protein components identical to the NADPH oxidase system responsible for the respiratory burst of phagocytes. In the present study we evaluated O2 sensing in mice with null mutant genotypes for two components of the phagocytic oxidase. Whole body plethysmography was used to study mice in an unanesthetized and unrestrained state. When exposed to an acute hypoxic stimulus, gp91phox null mutant mice and wild-type mice increased their minute ventilation (VE) by similar amounts. In contrast, p47phox null mutant mice demonstrated increases in VE in response to hypoxia that exceeded that of their wild-type counterparts (p47phox null mutant mice=98.0±18.0%, wild-type mice=20.0±13.0%, n=11, p=0.003). In vitro recordings of CSN activity demonstrated that resting (basal) neural activity was marginally elevated in p47phox null mutant mice. With hypoxic challenge, mean CSN discharge was 1.5-fold greater in p47phox null mutant mice as compared with wild-type mice (p47phox null mutant mice=109.61±13.29 imp./sec., wild-type mice=72.54±7.65 imp./sec., n=8&7, respectively, p=0.026). Consequently, the hypoxia-evoked CSN discharge (stimulus-basal) was nearly 58% larger in p47phox null mutant mice. When exposed to hypobaric hypoxia for 72 hours, gp91phox null mutant and p47phox null mutant mice both demonstrated similar quantities of epo mRNA in kidney as compared to their respective wild-type controls. These findings confirm the previous observation that absence of the gp91phox component of the phagocytic NADPH oxidase does not alter the O2 sensing mechanism of the carotid body. However, absence of the p47phox component significantly potentiates ventilatory and chemoreceptor responses to hypoxia. O2 sensing in epo producing cells of the kidney appears to be independent of both the gp91phox and p47phox components of the phagocytic NADPH oxidase.
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