Copyright © 2006, European Society of Cardiology
Oxygen sensors in hypoxic pulmonary vasoconstriction
University of Giessen Lung Center (UGLC), Medical Clinic II, Justus-Liebig-University Giessen, Klinikstrasse 36, 35392 Giessen, Germany
* Corresponding author. Tel.: +49 641 99 42351; fax: +49 641 99 42419. Email address: Norbert.Weissmann{at}UGLC.de Norbert.Weissmann{at}innere.med.uni-giessen.de
Hypoxic pulmonary vasoconstriction (HPV) is an essential mechanism adapting lung perfusion to regional ventilation. Perturbations to HPV, such as those occurring in pneumonia, acute respiratory distress syndrome and liver failure, can result in arterial hypoxemia. Under conditions of general hypoxia, HPV increases pulmonary vascular resistance and thus causes acute pulmonary hypertension. Despite intensive research, the underlying mechanisms of HPV have not been fully elucidated. Deciphering signalling pathways that result in HPV could suggest novel approaches to address a failure of HPV, as well as for the treatment of pulmonary hypertension associated with HPV. Within this context, this review focuses on current concepts in the oxygen sensing mechanisms that underlie HPV.
KEYWORDS Hypoxic pulmonary vasoconstriction; Oxygen; Oxygen sensing; Lung; Hypoxia
Time for primary review 22 days
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
E. Delannoy, A. Courtois, V. Freund-Michel, V. Leblais, R. Marthan, and B. Muller Hypoxia-induced hyperreactivity of pulmonary arteries: role of cyclooxygenase-2, isoprostanes, and thromboxane receptors Cardiovasc Res, September 16, 2009; (2009) cvp292v2. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Roth, M. Rupp, S. Hofmann, M. Mittal, B. Fuchs, N. Sommer, N. Parajuli, K. Quanz, D. Schubert, E. Dony, et al. Heme Oxygenase-2 and Large-Conductance Ca2+-activated K+ Channels: Lung Vascular Effects of Hypoxia Am. J. Respir. Crit. Care Med., August 15, 2009; 180(4): 353 - 364. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. D. Michelakis Soluble guanylate cyclase stimulators as a potential therapy for PAH: enthusiasm, pragmatism and concern Eur. Respir. J., April 1, 2009; 33(4): 717 - 721. [Full Text] [PDF] |
||||
![]() |
A. L. Firth, D. V. Gordienko, K. H. Yuill, and S. V. Smirnov Cellular localization of mitochondria contributes to Kv channel-mediated regulation of cellular excitability in pulmonary but not mesenteric circulation Am J Physiol Lung Cell Mol Physiol, March 1, 2009; 296(3): L347 - L360. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Schneider, I. Mitchell, N. Singhal, V. Kirk, and S. U. Hasan Prenatal Cigarette Smoke Exposure Attenuates Recovery from Hypoxemic Challenge in Preterm Infants Am. J. Respir. Crit. Care Med., September 1, 2008; 178(5): 520 - 526. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Weissmann Nitric Oxide-Mediated Zinc Release: A New (Modulatory) Pathway in Hypoxic Pulmonary Vasoconstriction Circ. Res., June 20, 2008; 102(12): 1451 - 1454. [Full Text] [PDF] |
||||
![]() |
W. Wu, O. Platoshyn, A. L. Firth, and J. X.-J. Yuan Hypoxia divergently regulates production of reactive oxygen species in human pulmonary and coronary artery smooth muscle cells Am J Physiol Lung Cell Mol Physiol, October 1, 2007; 293(4): L952 - L959. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Mittal, M. Roth, P. Konig, S. Hofmann, E. Dony, P. Goyal, A.-C. Selbitz, R. T. Schermuly, H. A. Ghofrani, G. Kwapiszewska, et al. Hypoxia-Dependent Regulation of Nonphagocytic NADPH Oxidase Subunit NOX4 in the Pulmonary Vasculature Circ. Res., August 3, 2007; 101(3): 258 - 267. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Weissmann, A. Dietrich, B. Fuchs, H. Kalwa, M. Ay, R. Dumitrascu, A. Olschewski, U. Storch, M. Mederos y Schnitzler, H. A. Ghofrani, et al. Classical transient receptor potential channel 6 (TRPC6) is essential for hypoxic pulmonary vasoconstriction and alveolar gas exchange PNAS, December 12, 2006; 103(50): 19093 - 19098. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Weissmann, F. Grimminger, and W. Seeger Hypoxia in lung vascular biology and disease Cardiovasc Res, September 1, 2006; 71(4): 618 - 619. [Full Text] [PDF] |
||||





