Abstract：
:In recent years, it has become evident that reactive oxygen species (ROS) play a critical role in the regulation of several physiological and pathophysiological processes. Herein we review the main sources, targets and pathophysiological roles of ROS in pulmonary vascular smooth muscle. Mitochondria and NADPH oxidases represent the major sources of ROS in vascular cells. In addition, ROS can be produced by different pathways of arachidonic acid metabolism, endothelial NO synthase (eNOS) and xantine oxidase. There is increasing evidence for the role of ROS, specially hydrogen peroxide, as signaling moieties to induce increase in intracellular calcium concentration ([Ca2+]i) and contraction in pulmonary artery smooth muscle cells (PASMC) through the modulation of a variety of targets, such as Rho kinases (ROCK), protein kinase C (PKC), voltage-gated potassium K+ (Kv) channels and ryanodine receptors (RyR). Thus, an increase in ROS has been reported to contribute to the responses induced by different vasoconstrictor stimuli, including hypoxia. Finally, results from recent studies highlighting the involvement of ROS in the development of pulmonary hypertension are discussed in the present paper.
journal_name
Respir Physiol Neurobioljournal_title
Respiratory physiology & neurobiologyauthors
Perez-Vizcaino F,Cogolludo A,Moreno Ldoi
10.1016/j.resp.2010.08.009subject
Has Abstractpub_date
2010-12-31 00:00:00pages
212-20issue
3eissn
1569-9048issn
1878-1519pii
S1569-9048(10)00313-7journal_volume
174pub_type
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