| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print June 30, 2002
J Appl Physiol, 10.1152/jap.00251.2002
Submitted on March 25, 2002
Accepted on June 24, 2002
1 Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA
* To whom correspondence should be addressed. E-mail: jwood2{at}kumc.edu.
Previous data from our laboratory suggest that systemic hypoxia results in microvascular oxidative stress due to a change in the balance between reactive oxygen species (ROS) and nitric oxide (NO), thereby promoting leukocyte-endothelial adhesive interactions. These experiments explored two alternative mechanisms to account for the altered ROS/NO balance during hypoxia: 1) decreased NO synthesis by nitric oxide synthase (NOS) due to limited O2 substrate availability, with the lower levels of the antioxidant NO leading to higher ROS concentrations, and 2) increased superoxide generation enhancing degradation of NO, which would lower tissue NO levels without impaired NO synthesis. The ROS levels and leukocyte-endothelial adhesive interactions in mesenteric venules of rats at various levels of systemic hypoxia were studied in the absence and presence of an NO donor (spermine NONOate, SNO) and of the NO precursor L-arginine. We hypothesized that if the lower NO levels during hypoxia were due to O2 substrate limitation, L-arginine would not prevent hypoxia-induced microvascular responses. Graded hypoxia (produced by breathing 15%, 10%, and 7.5% O2 gas mixtures) increased both ROS generation (123±6%, 148±11% and 167±3% of control values) and leukocyte adherence. ROS levels during breathing of 10% and 7.5% O2 were significantly attenuated to similar extents by SNO (105±6% and 108±3%, respectively) and by L-arginine (117±5% and 115±2%, respectively). Both interventions also significantly reduced hypoxia-induced leukocyte adherence to similar degrees. The fact that the effects of the NO precursor L-arginine were quantitatively similar to those of the NO donor do not support the idea that NO generation is impaired in hypoxia, and suggests that tissue NO levels are depleted by the increased ROS concentrations during hypoxia.
This article has been cited by other articles:
|
|
 |
|
  C. G. Julian, H. L. Galan, M. J. Wilson, W. DeSilva, D. Cioffi-Ragan, J. Schwartz, and L. G. Moore Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2008; 295(3): R906 - R915. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bertuglia Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1914 - H1922. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. C. Gonzalez, J. Allen, V. G. Blanco, E. J. Schmidt, N. van Rooijen, and J. G. Wood Alveolar macrophages are necessary for the systemic inflammation of acute alveolar hypoxia J Appl Physiol, October 1, 2007; 103(4): 1386 - 1394. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. L. Clanton Hypoxia-induced reactive oxygen species formation in skeletal muscle J Appl Physiol, June 1, 2007; 102(6): 2379 - 2388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. C. Gonzalez, J. Allen, E. J. Schmidt, A. J. Casillan, T. Orth, and J. G. Wood Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2285 - H2294. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Phillips, E. B. Olson, J. H. Lombard, and B. J. Morgan Chronic intermittent hypoxia alters NE reactivity and mechanics of skeletal muscle resistance arteries J Appl Physiol, April 1, 2006; 100(4): 1117 - 1123. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. E. Foster, D. C. McKenzie, W. K. Milsom, and A. W. Sheel Effects of two protocols of intermittent hypoxia on human ventilatory, cardiovascular and cerebral responses to hypoxia J. Physiol., September 1, 2005; 567(2): 689 - 699. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Orth, J. A. Allen, J. G. Wood, and N. C. Gonzalez Plasma from conscious hypoxic rats stimulates leukocyte-endothelial interactions in normoxic cremaster venules J Appl Physiol, July 1, 2005; 99(1): 290 - 297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. A. Orth, J. A. Allen, J. G. Wood, and N. C. Gonzalez Exercise training prevents the inflammatory response to hypoxia in cremaster venules J Appl Physiol, June 1, 2005; 98(6): 2113 - 2118. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Friesenecker, A. G. Tsai, M. W. Dunser, A. J. Mayr, J. Martini, H. Knotzer, W. Hasibeder, and M. Intaglietta Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1792 - H1800. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Phillips, I. Drenjancevic-Peric, J. C. Frisbee, and J. H. Lombard Chronic AT1 receptor blockade alters mechanisms mediating responses to hypoxia in rat skeletal muscle resistance arteries Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H545 - H552. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Phillips, E. B. Olson, B. J. Morgan, and J. H. Lombard Chronic intermittent hypoxia impairs endothelium-dependent dilation in rat cerebral and skeletal muscle resistance arteries Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H388 - H393. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Dix, T. Orth, J. Allen, J. G. Wood, and N. C. Gonzalez Activation of mast cells by systemic hypoxia, but not by local hypoxia, mediates increased leukocyte-endothelial adherence in cremaster venules J Appl Physiol, December 1, 2003; 95(6): 2495 - 2502. [Abstract] [Full Text]
|
|
|
|
 |
|
 N. N. C. Tam, Y. Gao, Y.-K. Leung, and S.-M. Ho Androgenic Regulation of Oxidative Stress in the Rat Prostate: Involvement of NAD(P)H Oxidases and Antioxidant Defense Machinery during Prostatic Involution and Regrowth Am. J. Pathol., December 1, 2003; 163(6): 2513 - 2522. [Abstract] [Full Text]
|
|
|
|
|
|
A. J. Casillan, N. C. Gonzalez, J. S. Johnson, D. R. S. Steiner, and J. G. Wood Mesenteric microvascular inflammatory responses to systemic hypoxia are mediated by PAF and LTB4 J Appl Physiol, June 1, 2003; 94(6): 2313 - 2322. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Shah, J. Allen, J. G. Wood, and N. C. Gonzalez Dissociation between skeletal muscle microvascular PO2 and hypoxia-induced microvascular inflammation J Appl Physiol, June 1, 2003; 94(6): 2323 - 2329. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. S. Steiner, N. C. Gonzalez, and J. G. Wood Mast cells mediate the microvascular inflammatory response to systemic hypoxia J Appl Physiol, January 1, 2003; 94(1): 325 - 334. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bertuglia and A. Giusti Role of nitric oxide in capillary perfusion and oxygen delivery regulation during systemic hypoxia Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H525 - H531. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
