Journal article
Authors list: Fuchs, Beate; Sommer, Natascha; Dietrich, Alexander; Schermuly, Ralph Theo; Ghofrani, Hossein Ardeschir; Grimminger, Friedrich; Seeger, Werner; Gudermann, Thomas; Weissmann, Norbert
Publication year: 2010
Pages: 282-291
Journal: Respiratory Physiology & Neurobiology
Volume number: 174
Issue number: 3
ISSN: 1569-9048
eISSN: 1878-1519
DOI Link: https://doi.org/10.1016/j.resp.2010.08.013
Publisher: Elsevier
Abstract:
Hypoxic pulmonary vasoconstriction (HPV) is an essential physiological mechanism of the lung that matches blood perfusion with alveolar ventilation to optimize gas exchange. Perturbations of HPV, as may occur in pneumonia or adult respiratory distress syndrome, can cause life-threatening hypoxemia. Despite intensive research for decades, the molecular mechanisms of HPV have not been fully elucidated. Reactive oxygen species (ROS) and changes in the cellular redox state are proposed to link O-2 sensing and pulmonary arterial smooth muscle cell contraction underlying HPV. In this regard, mitochondria and NAD(P)H oxidases are discussed as sources of ROS. However, there is controversy whether ROS levels decrease or increase during hypoxia. With this background we summarize the current knowledge on the role of ROS and redox state in HPV. (C) 2010 Elsevier B.V. All rights reserved.
Citation Styles
Harvard Citation style: Fuchs, B., Sommer, N., Dietrich, A., Schermuly, R., Ghofrani, H., Grimminger, F., et al. (2010) Redox signaling and reactive oxygen species in hypoxic pulmonary vasoconstriction, Respiratory Physiology & Neurobiology, 174(3), pp. 282-291. https://doi.org/10.1016/j.resp.2010.08.013
APA Citation style: Fuchs, B., Sommer, N., Dietrich, A., Schermuly, R., Ghofrani, H., Grimminger, F., Seeger, W., Gudermann, T., & Weissmann, N. (2010). Redox signaling and reactive oxygen species in hypoxic pulmonary vasoconstriction. Respiratory Physiology & Neurobiology. 174(3), 282-291. https://doi.org/10.1016/j.resp.2010.08.013
Keywords
ARTERIAL SMOOTH-MUSCLE; CAPACITATIVE CALCIUM-ENTRY; CYTOSOLIC PHOSPHOLIPASE A(2); GATED K+ CHANNELS; GUANYLATE-CYCLASE; INTRACELLULAR CA2+; INTRAPULMONARY ARTERIES; NADPH OXIDASE-INHIBITORS; pulmonary vasculature; REDOX STATE; SUPEROXIDE ANION