Pulmonary Hypertension Is a Probable NO-ONOO− Cycle Disease: A ReviewReportar como inadecuado




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ISRN Hypertension - Volume 2013 2013, Article ID 742418, 27 pages -

Review ArticleWashington State University, 638 NE 41st Avenue, Portland, OR 97232-3312, USA

Received 23 April 2012; Accepted 22 May 2012

Academic Editors: D.-P. Li and B. Waeber

Copyright © 2013 Martin L. Pall. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The NO-ONOO

cycle is a primarily local biochemical-physiological vicious cycle that appears to cause a series of chronic inflammatory diseases. This paper focuses on whether the cycle causes pulmonary arterial hypertension PAH when located in the pulmonary arteries. The cycle involves 12 elements, including superoxide, peroxynitrite ONOO

, nitric oxide NO, oxidative stress, NF-κB, inflammatory cytokines, iNOS, mitochondrial dysfunction, intracellular calcium, tetrahydrobiopterin depletion, NMDA activity, and TRP receptor activity. 10 of the 12 are elevated in PAH NMDA?, NO? and 11 have documented causal roles in PAH. Each stressor that initiates cases of PAH acts to raise cycle elements, and may, therefore, initiate the cycle in this way. PAH involves a primarily local mechanism as required by the cycle and the symptoms and signs of PAH are generated by elements of the cycle. Endothelin-1, which acts as a causal factor in PAH, acts as part of the cycle; its synthesis is stimulated by cycle elements, and it, in turn, increases each element of the cycle. This extraordinary fit to the principles of the NO-ONOO

cycle allows one to conclude that PAH is a NO-ONOO

cycle disease, and this fit supports the cycle as a major paradigm of chronic inflammatory disease.





Autor: Martin L. Pall

Fuente: https://www.hindawi.com/



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