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Am J Physiol Heart Circ Physiol (January 5, 2007). doi:10.1152/ajpheart.00981.2006
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Submitted on September 8, 2006
Accepted on January 4, 2007

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia

Norberto C. Gonzalez1*, Julie Allen1, Eric J. Schmidt1, Alfred J Casillan2, Teresa Orth2, and John G. Wood2

1 Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, United States
2 Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, United States

* To whom correspondence should be addressed. E-mail: ngonzale{at}kumc.edu.

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular PO2 and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried mediator. This study investigates the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANGIIRB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANGII on normoxic cremasters, suggesting ANGII generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANGIIRB blocked the leukocyte endothelial adherence produced by the MC secretagogue c48/80. These results suggest that the mediator contained in PAHR activates MC and stimulates the RAS leading to inflammation, and imply an RAS role in AH-induced inflammation




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J. Chao, J. G. Wood, V. G. Blanco, and N. C. Gonzalez
The Systemic Inflammation of Alveolar Hypoxia Is Initiated by Alveolar Macrophage-Borne Mediator(s)
Am. J. Respir. Cell Mol. Biol., November 1, 2009; 41(5): 573 - 582.
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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.
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