The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform
Norbert Weissmann - One of the best experts on this subject based on the ideXlab platform.
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Hypoxic Pulmonary Vasoconstriction in isolated mouse Pulmonary arterial vessels
Experimental Physiology, 2018Co-Authors: Ievgen Strielkov, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Natascha Sommer, Alexander Dietrich, Thomas Gudermann, Nicole C Krause, Norbert WeissmannAbstract:NEW FINDINGS: What is the central question of this study? Hypoxic Pulmonary Vasoconstriction has never been characterized in isolated mouse Pulmonary arteries of different generations in detail. What is the main finding and its importance? We found that only small intraPulmonary arteries (80-200 μm in diameter) exhibit Hypoxic Pulmonary Vasoconstriction. The observed response was sustained, significantly potentiated by depolarization-induced preconstriction and not dependent on the endothelium or TRPC6 channels. ABSTRACT: Hypoxic Pulmonary Vasoconstriction (HPV) is a physiological response of Pulmonary arteries, which adapts lung perfusion to regional ventilation. The properties of HPV vary significantly between animal species. Despite extensive use of mouse models in studies of HPV, this physiological response has never been characterized in isolated mouse Pulmonary arteries in detail. Using wire myography, we investigated the effect of 80 min exposure to hypoxia on the tone in mouse Pulmonary arteries of different generations in the presence and absence of preconstriction. Hypoxia induced a sustained relaxation in non-preconstricted extraPulmonary arteries (500-700 μm in diameter), but not in the presence of KCl-induced preconstriction. Large intraPulmonary arteries (450-650 μm in diameter) did not exhibit a significant response to the Hypoxic challenge. In contrast, in small intraPulmonary arteries (80-200 μm in diameter), hypoxia elicited a slowly developing sustained constriction, which was independent of the endothelium. The response was significantly potentiated in arteries preconstricted with KCl, but not with U46619. Hypoxic Pulmonary Vasoconstriction was not altered in Pulmonary arteries of TRPC6-deficient mice, which suggests that this response corresponds to the sustained phase of biphasic HPV observed earlier in isolated, buffer-perfused and ventilated mouse lungs. In conclusion, we have established a protocol that allows the study of sustained HPV in isolated mouse Pulmonary arteries. The data obtained might be useful for future studies of the mechanisms of HPV in mice.
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Recent advances in oxygen sensing and signal transduction in Hypoxic Pulmonary Vasoconstriction
Journal of Applied Physiology, 2017Co-Authors: Ievgen Strielkov, Natascha Sommer, Norbert WeissmannAbstract:Hypoxic Pulmonary Vasoconstriction (HPV) is a physiological reaction, which adapts lung perfusion to regional ventilation and optimizes gas exchange. Impaired HPV may cause systemic hypoxemia, whil...
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nebulization of the acidified sodium nitrite formulation attenuates acute Hypoxic Pulmonary Vasoconstriction
Respiratory Research, 2010Co-Authors: Bakytbek Egemnazarov, Bhola K Dahal, Garry T Elliott, Niel C Hoglen, Mark W Surber, Norbert Weissmann, Ralph T. Schermuly, F Grimminger, Werner Seeger, Hossein Ardeschir GhofraniAbstract:Background Generalized Hypoxic Pulmonary Vasoconstriction (HPV) occurring during exposure to hypoxia is a detrimental process resulting in an increase in lung vascular resistance. Nebulization of sodium nitrite has been shown to inhibit HPV. The aim of this project was to investigate and compare the effects of nebulization of nitrite and different formulations of acidified sodium nitrite on acute HPV.
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regulation of Hypoxic Pulmonary Vasoconstriction basic mechanisms
European Respiratory Journal, 2008Co-Authors: Natascha Sommer, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Werner Seeger, Alexander Dietrich, Thomas Gudermann, Rainer Schulz, Norbert WeissmannAbstract:Hypoxic Pulmonary Vasoconstriction (HPV), also known as the von Euler–Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes Pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure. Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised Vasoconstriction of the Pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to Pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltage-dependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of Hypoxic Pulmonary Vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate. In this context the present article focuses on the basic mechanisms of Hypoxic Pulmonary Vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of Hypoxic Pulmonary Vasoconstriction. SERIES “HYPOXIA: ERS LUNG SCIENCE CONFERENCE” Edited by N. Weissmann Number 6 in this Series
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oxygen sensors in Hypoxic Pulmonary Vasoconstriction
Cardiovascular Research, 2006Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Natascha Sommer, F GrimmingerAbstract: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.
Hossein Ardeschir Ghofrani - One of the best experts on this subject based on the ideXlab platform.
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Hypoxic Pulmonary Vasoconstriction in isolated mouse Pulmonary arterial vessels
Experimental Physiology, 2018Co-Authors: Ievgen Strielkov, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Natascha Sommer, Alexander Dietrich, Thomas Gudermann, Nicole C Krause, Norbert WeissmannAbstract:NEW FINDINGS: What is the central question of this study? Hypoxic Pulmonary Vasoconstriction has never been characterized in isolated mouse Pulmonary arteries of different generations in detail. What is the main finding and its importance? We found that only small intraPulmonary arteries (80-200 μm in diameter) exhibit Hypoxic Pulmonary Vasoconstriction. The observed response was sustained, significantly potentiated by depolarization-induced preconstriction and not dependent on the endothelium or TRPC6 channels. ABSTRACT: Hypoxic Pulmonary Vasoconstriction (HPV) is a physiological response of Pulmonary arteries, which adapts lung perfusion to regional ventilation. The properties of HPV vary significantly between animal species. Despite extensive use of mouse models in studies of HPV, this physiological response has never been characterized in isolated mouse Pulmonary arteries in detail. Using wire myography, we investigated the effect of 80 min exposure to hypoxia on the tone in mouse Pulmonary arteries of different generations in the presence and absence of preconstriction. Hypoxia induced a sustained relaxation in non-preconstricted extraPulmonary arteries (500-700 μm in diameter), but not in the presence of KCl-induced preconstriction. Large intraPulmonary arteries (450-650 μm in diameter) did not exhibit a significant response to the Hypoxic challenge. In contrast, in small intraPulmonary arteries (80-200 μm in diameter), hypoxia elicited a slowly developing sustained constriction, which was independent of the endothelium. The response was significantly potentiated in arteries preconstricted with KCl, but not with U46619. Hypoxic Pulmonary Vasoconstriction was not altered in Pulmonary arteries of TRPC6-deficient mice, which suggests that this response corresponds to the sustained phase of biphasic HPV observed earlier in isolated, buffer-perfused and ventilated mouse lungs. In conclusion, we have established a protocol that allows the study of sustained HPV in isolated mouse Pulmonary arteries. The data obtained might be useful for future studies of the mechanisms of HPV in mice.
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nebulization of the acidified sodium nitrite formulation attenuates acute Hypoxic Pulmonary Vasoconstriction
Respiratory Research, 2010Co-Authors: Bakytbek Egemnazarov, Bhola K Dahal, Garry T Elliott, Niel C Hoglen, Mark W Surber, Norbert Weissmann, Ralph T. Schermuly, F Grimminger, Werner Seeger, Hossein Ardeschir GhofraniAbstract:Background Generalized Hypoxic Pulmonary Vasoconstriction (HPV) occurring during exposure to hypoxia is a detrimental process resulting in an increase in lung vascular resistance. Nebulization of sodium nitrite has been shown to inhibit HPV. The aim of this project was to investigate and compare the effects of nebulization of nitrite and different formulations of acidified sodium nitrite on acute HPV.
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regulation of Hypoxic Pulmonary Vasoconstriction basic mechanisms
European Respiratory Journal, 2008Co-Authors: Natascha Sommer, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Werner Seeger, Alexander Dietrich, Thomas Gudermann, Rainer Schulz, Norbert WeissmannAbstract:Hypoxic Pulmonary Vasoconstriction (HPV), also known as the von Euler–Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes Pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure. Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised Vasoconstriction of the Pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to Pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltage-dependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of Hypoxic Pulmonary Vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate. In this context the present article focuses on the basic mechanisms of Hypoxic Pulmonary Vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of Hypoxic Pulmonary Vasoconstriction. SERIES “HYPOXIA: ERS LUNG SCIENCE CONFERENCE” Edited by N. Weissmann Number 6 in this Series
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oxygen sensors in Hypoxic Pulmonary Vasoconstriction
Cardiovascular Research, 2006Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Natascha Sommer, F GrimmingerAbstract: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.
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Evidence for a role of protein kinase C in Hypoxic Pulmonary Vasoconstriction
American Journal of Physiology-lung Cellular and Molecular Physiology, 1999Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Robert Voswinckel, Thorsten Hardebusch, Simone Rosseau, F GrimmingerAbstract:Hypoxic Pulmonary Vasoconstriction (HPV) matches lung perfusion to ventilation, thus optimizing gas exchange. NADPH oxidase-related superoxide anion generation has been suggested as part of the sig...
F Grimminger - One of the best experts on this subject based on the ideXlab platform.
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Hypoxic Pulmonary Vasoconstriction in isolated mouse Pulmonary arterial vessels
Experimental Physiology, 2018Co-Authors: Ievgen Strielkov, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Natascha Sommer, Alexander Dietrich, Thomas Gudermann, Nicole C Krause, Norbert WeissmannAbstract:NEW FINDINGS: What is the central question of this study? Hypoxic Pulmonary Vasoconstriction has never been characterized in isolated mouse Pulmonary arteries of different generations in detail. What is the main finding and its importance? We found that only small intraPulmonary arteries (80-200 μm in diameter) exhibit Hypoxic Pulmonary Vasoconstriction. The observed response was sustained, significantly potentiated by depolarization-induced preconstriction and not dependent on the endothelium or TRPC6 channels. ABSTRACT: Hypoxic Pulmonary Vasoconstriction (HPV) is a physiological response of Pulmonary arteries, which adapts lung perfusion to regional ventilation. The properties of HPV vary significantly between animal species. Despite extensive use of mouse models in studies of HPV, this physiological response has never been characterized in isolated mouse Pulmonary arteries in detail. Using wire myography, we investigated the effect of 80 min exposure to hypoxia on the tone in mouse Pulmonary arteries of different generations in the presence and absence of preconstriction. Hypoxia induced a sustained relaxation in non-preconstricted extraPulmonary arteries (500-700 μm in diameter), but not in the presence of KCl-induced preconstriction. Large intraPulmonary arteries (450-650 μm in diameter) did not exhibit a significant response to the Hypoxic challenge. In contrast, in small intraPulmonary arteries (80-200 μm in diameter), hypoxia elicited a slowly developing sustained constriction, which was independent of the endothelium. The response was significantly potentiated in arteries preconstricted with KCl, but not with U46619. Hypoxic Pulmonary Vasoconstriction was not altered in Pulmonary arteries of TRPC6-deficient mice, which suggests that this response corresponds to the sustained phase of biphasic HPV observed earlier in isolated, buffer-perfused and ventilated mouse lungs. In conclusion, we have established a protocol that allows the study of sustained HPV in isolated mouse Pulmonary arteries. The data obtained might be useful for future studies of the mechanisms of HPV in mice.
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nebulization of the acidified sodium nitrite formulation attenuates acute Hypoxic Pulmonary Vasoconstriction
Respiratory Research, 2010Co-Authors: Bakytbek Egemnazarov, Bhola K Dahal, Garry T Elliott, Niel C Hoglen, Mark W Surber, Norbert Weissmann, Ralph T. Schermuly, F Grimminger, Werner Seeger, Hossein Ardeschir GhofraniAbstract:Background Generalized Hypoxic Pulmonary Vasoconstriction (HPV) occurring during exposure to hypoxia is a detrimental process resulting in an increase in lung vascular resistance. Nebulization of sodium nitrite has been shown to inhibit HPV. The aim of this project was to investigate and compare the effects of nebulization of nitrite and different formulations of acidified sodium nitrite on acute HPV.
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regulation of Hypoxic Pulmonary Vasoconstriction basic mechanisms
European Respiratory Journal, 2008Co-Authors: Natascha Sommer, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Werner Seeger, Alexander Dietrich, Thomas Gudermann, Rainer Schulz, Norbert WeissmannAbstract:Hypoxic Pulmonary Vasoconstriction (HPV), also known as the von Euler–Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes Pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure. Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised Vasoconstriction of the Pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to Pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltage-dependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of Hypoxic Pulmonary Vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate. In this context the present article focuses on the basic mechanisms of Hypoxic Pulmonary Vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of Hypoxic Pulmonary Vasoconstriction. SERIES “HYPOXIA: ERS LUNG SCIENCE CONFERENCE” Edited by N. Weissmann Number 6 in this Series
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oxygen sensors in Hypoxic Pulmonary Vasoconstriction
Cardiovascular Research, 2006Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Natascha Sommer, F GrimmingerAbstract: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.
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Hypoxic Pulmonary Vasoconstriction: a multifactorial response?
American Journal of Physiology-lung Cellular and Molecular Physiology, 2001Co-Authors: Norbert Weissmann, F Grimminger, Andrea Olschewski, Werner SeegerAbstract:Hypoxic Pulmonary Vasoconstriction (HPV) is an essential mechanism that matches lung perfusion to ventilation to optimize Pulmonary gas exchange (for reviews, see Refs. [9][1], [28][2], [31][3]). Even if early reports observed that alveolar hypoxia induces Pulmonary arterial hypertension, the modern
Ralph T. Schermuly - One of the best experts on this subject based on the ideXlab platform.
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Hypoxic Pulmonary Vasoconstriction in isolated mouse Pulmonary arterial vessels
Experimental Physiology, 2018Co-Authors: Ievgen Strielkov, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Natascha Sommer, Alexander Dietrich, Thomas Gudermann, Nicole C Krause, Norbert WeissmannAbstract:NEW FINDINGS: What is the central question of this study? Hypoxic Pulmonary Vasoconstriction has never been characterized in isolated mouse Pulmonary arteries of different generations in detail. What is the main finding and its importance? We found that only small intraPulmonary arteries (80-200 μm in diameter) exhibit Hypoxic Pulmonary Vasoconstriction. The observed response was sustained, significantly potentiated by depolarization-induced preconstriction and not dependent on the endothelium or TRPC6 channels. ABSTRACT: Hypoxic Pulmonary Vasoconstriction (HPV) is a physiological response of Pulmonary arteries, which adapts lung perfusion to regional ventilation. The properties of HPV vary significantly between animal species. Despite extensive use of mouse models in studies of HPV, this physiological response has never been characterized in isolated mouse Pulmonary arteries in detail. Using wire myography, we investigated the effect of 80 min exposure to hypoxia on the tone in mouse Pulmonary arteries of different generations in the presence and absence of preconstriction. Hypoxia induced a sustained relaxation in non-preconstricted extraPulmonary arteries (500-700 μm in diameter), but not in the presence of KCl-induced preconstriction. Large intraPulmonary arteries (450-650 μm in diameter) did not exhibit a significant response to the Hypoxic challenge. In contrast, in small intraPulmonary arteries (80-200 μm in diameter), hypoxia elicited a slowly developing sustained constriction, which was independent of the endothelium. The response was significantly potentiated in arteries preconstricted with KCl, but not with U46619. Hypoxic Pulmonary Vasoconstriction was not altered in Pulmonary arteries of TRPC6-deficient mice, which suggests that this response corresponds to the sustained phase of biphasic HPV observed earlier in isolated, buffer-perfused and ventilated mouse lungs. In conclusion, we have established a protocol that allows the study of sustained HPV in isolated mouse Pulmonary arteries. The data obtained might be useful for future studies of the mechanisms of HPV in mice.
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nebulization of the acidified sodium nitrite formulation attenuates acute Hypoxic Pulmonary Vasoconstriction
Respiratory Research, 2010Co-Authors: Bakytbek Egemnazarov, Bhola K Dahal, Garry T Elliott, Niel C Hoglen, Mark W Surber, Norbert Weissmann, Ralph T. Schermuly, F Grimminger, Werner Seeger, Hossein Ardeschir GhofraniAbstract:Background Generalized Hypoxic Pulmonary Vasoconstriction (HPV) occurring during exposure to hypoxia is a detrimental process resulting in an increase in lung vascular resistance. Nebulization of sodium nitrite has been shown to inhibit HPV. The aim of this project was to investigate and compare the effects of nebulization of nitrite and different formulations of acidified sodium nitrite on acute HPV.
-
regulation of Hypoxic Pulmonary Vasoconstriction basic mechanisms
European Respiratory Journal, 2008Co-Authors: Natascha Sommer, Ralph T. Schermuly, F Grimminger, Hossein Ardeschir Ghofrani, Werner Seeger, Alexander Dietrich, Thomas Gudermann, Rainer Schulz, Norbert WeissmannAbstract:Hypoxic Pulmonary Vasoconstriction (HPV), also known as the von Euler–Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes Pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure. Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised Vasoconstriction of the Pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to Pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltage-dependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of Hypoxic Pulmonary Vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate. In this context the present article focuses on the basic mechanisms of Hypoxic Pulmonary Vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of Hypoxic Pulmonary Vasoconstriction. SERIES “HYPOXIA: ERS LUNG SCIENCE CONFERENCE” Edited by N. Weissmann Number 6 in this Series
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oxygen sensors in Hypoxic Pulmonary Vasoconstriction
Cardiovascular Research, 2006Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Natascha Sommer, F GrimmingerAbstract: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.
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Evidence for a role of protein kinase C in Hypoxic Pulmonary Vasoconstriction
American Journal of Physiology-lung Cellular and Molecular Physiology, 1999Co-Authors: Norbert Weissmann, Ralph T. Schermuly, Hossein Ardeschir Ghofrani, Werner Seeger, Robert Voswinckel, Thorsten Hardebusch, Simone Rosseau, F GrimmingerAbstract:Hypoxic Pulmonary Vasoconstriction (HPV) matches lung perfusion to ventilation, thus optimizing gas exchange. NADPH oxidase-related superoxide anion generation has been suggested as part of the sig...
Stephen L Archer - One of the best experts on this subject based on the ideXlab platform.
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counterpoint Hypoxic Pulmonary Vasoconstriction is not mediated by increased production of reactive oxygen species
Journal of Applied Physiology, 2006Co-Authors: Kenneth E Weir, Stephen L ArcherAbstract:The acute Hypoxic Pulmonary Vasoconstriction (HPV) that we discuss in this debate involves rapid constriction of small Pulmonary arteries in response to physiological levels of alveolar hypoxia. HPV starts within seconds of the onset of Hypoxic ventilation and we focus on the early events before
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Hypoxic Pulmonary Vasoconstriction
Journal of Applied Physiology, 2005Co-Authors: Rohit Moudgil, Evangelos D Michelakis, Stephen L ArcherAbstract:Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, through disease, and by desire, in our quest for altitude. Hypoxic Pulmonary Vasoconstriction (HPV) is a widely con...
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Redox Regulation of K+ Channels and Hypoxic Pulmonary Vasoconstriction
Ion Flux in Pulmonary Vascular Control, 1993Co-Authors: J M Post, Stephen L Archer, E. K. Weir, Joseph R HumeAbstract:The Pulmonary vasculature is unique in that hypoxia causes Vasoconstriction; whereas, most systemic vessels dilate (Daut et al., 1990). Hypoxic Pulmonary Vasoconstriction (HPV) serves as an adaptive mechanism by which blood flow is diverted from poorly ventilated to better ventilated regions of the lung to optimize ventilation/perfusion matching (Archer and Weir, 1989a; Cutaia and Rounds, 1990).
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direct role for potassium channel inhibition in Hypoxic Pulmonary Vasoconstriction
American Journal of Physiology-cell Physiology, 1992Co-Authors: J M Post, Stephen L Archer, Joseph R Hume, E K WeirAbstract:Cellular mechanisms responsible for Hypoxic Pulmonary Vasoconstriction were investigated in Pulmonary arterial cells, isolated perfused lung, and Pulmonary artery rings. Three K+ channel antagonist...