Role of erythropoietin in adaptation to hypoxia

1990 ◽  
Vol 46 (11-12) ◽  
pp. 1197-1201 ◽  
Author(s):  
H. Scholz ◽  
H. -J. Schurek ◽  
K. -U. Eckardt ◽  
C. Bauer
Keyword(s):  
Adaptation To Hypoxia

scholarly journals A2B adenosine receptor dampens hypoxia-induced vascular leak

Blood ◽  
2008 ◽  
Vol 111 (4) ◽  
pp. 2024-2035 ◽  
Author(s):  
Tobias Eckle ◽  
Marion Faigle ◽  
Almut Grenz ◽  
Stefanie Laucher ◽  
Linda F. Thompson ◽  
...  
Keyword(s):  
Control Point ◽  
Fold Increase ◽  
Vascular Leakage ◽  
Adaptation To Hypoxia ◽  
Vascular Leak ◽  
Extracellular Adenosine ◽  
Fold Reduction ◽  
Complete Reversal

Extracellular adenosine has been implicated in adaptation to hypoxia and previous studies demonstrated a central role in vascular responses. Here, we examined the contribution of individual adenosine receptors (ARs: A1AR/A2AAR/A2BAR/A3AR) to vascular leak induced by hypoxia. Initial profiling studies revealed that siRNA-mediated repression of the A2BAR selectively increased endothelial leak in response to hypoxia in vitro. In parallel, vascular permeability was significantly increased in vascular organs of A2BAR−/−-mice subjected to ambient hypoxia (8% oxygen, 4 hours; eg, lung: 2.1 ± 0.12-fold increase). By contrast, hypoxia-induced vascular leak was not accentuated in A1AR−/−-, A2AAR−/−-, or A3AR−/−-deficient mice, suggesting a degree of specificity for the A2BAR. Further studies in wild type mice revealed that the selective A2BAR antagonist PSB1115 resulted in profound increases in hypoxia-associated vascular leakage while A2BAR agonist (BAY60-6583 [2-[6-amino-3,5-dicyano-4-[4-(cyclopropylmethoxy)-. phenyl]pyridin-2-ylsulfanyl]acetamide]) treatment was associated with almost complete reversal of hypoxia-induced vascular leakage (eg, lung: 2.0 ± 0.21-fold reduction). Studies in bone marrow chimeric A2BAR mice suggested a predominant role of vascular A2BARs in this response, while hypoxia-associated increases in tissue neutrophils were, at least in part, mediated by A2BAR expressing hematopoietic cells. Taken together, these studies provide pharmacologic and genetic evidence for vascular A2BAR signaling as central control point of hypoxia-associated vascular leak.

scholarly journals The mitochondrial ATP-dependent potassium channel and its pharmacological modulators

2016 ◽  
Vol 14 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Elena V Pogilova ◽  
Vasiliy E Novikov ◽  
Olga S Levchenkova
Keyword(s):  
Potassium Channel ◽  
The State ◽  
Adaptation To Hypoxia ◽  
Metabolic Processes ◽  
Cell Adaptation ◽  
Pharmacological Modulation ◽  
Pharmacological Modulators

This review is devoted to analysis of current research about the role of mitochondrial ATP-dependent potassium channel (mitoКАТP) in the regulation of metabolic processes of the cell. The mechanisms of cell adaptation to hypoxia and ischemia involving mitoКАТP is considered in the article. The opportunity of pharmacological modulation of mitoКАТP activity to stimulate processes of cell adaptation to damaging factors is discussed. This approach seems promising for the development of effective pharmacotherapy of diseases which have in their pathogenesis the state of hypoxia and ischemia.

scholarly journals The role of nitrogen oxides in human adaptation to hypoxia

2011 ◽  
Vol 1 (1) ◽  
Author(s):  
Denny Z. Levett ◽  
◽  
Bernadette O. Fernandez ◽  
Heather L. Riley ◽  
Daniel S. Martin ◽  
...  
Keyword(s):  
Nitrogen Oxides ◽  
Adaptation To Hypoxia ◽  
Human Adaptation

scholarly journals Adaptation to Hypoxia Prevents Beta‐Amyloid (Ab) Toxicity: Role of Nitric Oxide

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Eugenia B. Manukhina ◽  
Maya G. Pshennikova ◽  
Svetlana Yu. Mashina ◽  
Anna V. Goryacheva ◽  
Dmitry A. Pokidyshev ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Beta Amyloid ◽  
Adaptation To Hypoxia

scholarly journals Author response: Cardiovascular adaptation to hypoxia and the role of peripheral resistance

2017 ◽  
Author(s):  
Andrew S Cowburn ◽  
David Macias ◽  
Charlotte Summers ◽  
Edwin R Chilvers ◽  
Randall S Johnson
Keyword(s):  
Peripheral Resistance ◽  
Author Response ◽  
Adaptation To Hypoxia

scholarly journals GRK2-Dependent HuR Phosphorylation Regulates HIF1α Activation under Hypoxia or Adrenergic Stress

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1216
Author(s):  
Clara Reglero ◽  
Vanesa Lafarga ◽  
Verónica Rivas ◽  
Ángela Albitre ◽  
Paula Ramos ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Luminal Breast Cancer ◽  
Adaptation To Hypoxia ◽  
Receptor Kinase ◽  
Breast Cancer Patients ◽  
Mrna Binding Protein ◽  
Relevant Role ◽  
Mrna Binding ◽  
G Protein Coupled

Adaptation to hypoxia is a common feature in solid tumors orchestrated by oxygen-dependent and independent upregulation of the hypoxia-inducible factor-1α (HIF-1α). We unveiled that G protein-coupled receptor kinase (GRK2), known to be overexpressed in certain tumors, fosters this hypoxic pathway via phosphorylation of the mRNA-binding protein HuR, a central HIF-1α modulator. GRK2-mediated HuR phosphorylation increases the total levels and cytoplasmic shuttling of HuR in response to hypoxia, and GRK2-phosphodefective HuR mutants show defective cytosolic accumulation and lower binding to HIF-1α mRNA in hypoxic Hela cells. Interestingly, enhanced GRK2 and HuR expression correlate in luminal breast cancer patients. GRK2 also promotes the HuR/HIF-1α axis and VEGF-C accumulation in normoxic MCF7 breast luminal cancer cells and is required for the induction of HuR/HIF1-α in response to adrenergic stress. Our results point to a relevant role of the GRK2/HuR/HIF-1α module in the adaptation of malignant cells to tumor microenvironment-related stresses.

scholarly journals The influence of altitude hypoxia on uroflowmetry parameters in women

2016 ◽  
Vol 311 (3) ◽  
pp. F562-F566 ◽  
Author(s):  
Vittore Verratti ◽  
Luana Paulesu ◽  
Tiziana Pietrangelo ◽  
Christian Doria ◽  
Camillo Di Giulio ◽  
...  
Keyword(s):  
Scientific Evidence ◽  
Flow Time ◽  
Adaptation To Hypoxia ◽  
Adult Women ◽  
Flow Volume ◽  
Altitude Hypoxia ◽  
Hypoxic Conditions ◽  
Time Flow ◽  
New Strategies

There is scientific evidence to suggest a correlation between hypoxia and the physiology of micturition. During a Himalayan Scientific and Mountaineering Expedition, we performed tests to investigate the functional interactions between altitude hypoxia and uroflowmetry parameters in women. The tests were carried out in seven women (36.3 ± 7.1 yr) from normoxic [1,340 meters above sea level (m a.s.l.)] to hypoxic conditions (up to 5,050 m a.s.l.) and during the return descent. The following measures were determined: uroflowmetry parameters and saturation of peripheral oxygen (SpO2). As expected, SpO2 decreased from 97.7 to 77.8% with increasing altitude. Micturition flow time, flow volume, and voiding time increased with altitude ( P < 0.04 for all), indicating a negative correlation with SpO2. In conclusion, in young adult women, micturition physiological parameters were affected during adaptation to hypoxia; the correlation with SpO2 strongly suggests a role of hypoxia in these changes. These data could help to support the design of new strategies for both prevention and medical treatment. An example of the latter might be hyperbaric oxygen therapy, which in some studies has proved able to reduce the symptoms in patients with hypoxic bladder.

The heart as an endocrine organ

2012 ◽  
Vol 153 (51) ◽  
pp. 2041-2047
Author(s):  
Emese Mezősi ◽  
László Bajnok ◽  
Kálmán Tóth
Keyword(s):  
Volume Overload ◽  
Adaptation To Hypoxia ◽  
Primary Role ◽  
Human Beings ◽  
Hormone Production ◽  
Complex Relation ◽  
Organ Systems ◽  
Aldosterone Production ◽  
Mechanical Pump

The discovery of cardiac hormone production significantly changed the evaluation of the function of the heart, which is rather regarded as a determining factor of the electrolyte and hemodynamic homeostasis cooperating with other organ systems instead of a mechanical pump. The most important hormones produced by the heart are the natriuretic peptides that have the primary role of protection against volume overload through natriuretic, diuretic, vasodilator and antiproliferative effects. They are integrative markers of the cardiac, vascular and renal functions and marking cardiorenal distress. Brain natriuretic peptide and the N-terminal pro-hormone (NT-proBNP) became generally accepted markers of heart failure exceeding traditional pathophysiological significance of those. They are useful in the diagnosis, estimation of prognosis and therapy guidance and their therapeutic administration is also available. Although the detection of extraadrenal aldosterone production is an exciting new discovery, intracardial aldosterone production is not significant in human beings. The intracardial thyroid hormone production is regulated by deiodinase activity. The role of elevated T3 concentration was suggested in the development of cardiac hypertrophy, while low T3 is assumed to be important in adaptation to hypoxia. An unexpected, complex relation can be determined between epicardial adipose tissue and coronary artery diseases, cytokine and adipokine production of adipocytes might be a part of the self-enhancing process of atherosclerosis. Orv. Hetil., 2012, 153, 2041–2047.

scholarly journals Oxygen sensing by the carotid body: mechanisms and role in adaptation to hypoxia

2016 ◽  
Vol 310 (8) ◽  
pp. C629-C642 ◽  
Author(s):  
José López-Barneo ◽  
Patricia González-Rodríguez ◽  
Lin Gao ◽  
M. Carmen Fernández-Agüera ◽  
Ricardo Pardal ◽  
...  
Keyword(s):  
Carotid Body ◽  
Close Contact ◽  
Nerve Fibers ◽  
Whole Body ◽  
Adaptation To Hypoxia ◽  
Glomus Cells ◽  
Adaptive Processes ◽  
Cell Depolarization ◽  
Sensory Fibers

Oxygen (O2) is fundamental for cell and whole-body homeostasis. Our understanding of the adaptive processes that take place in response to a lack of O2 (hypoxia) has progressed significantly in recent years. The carotid body (CB) is the main arterial chemoreceptor that mediates the acute cardiorespiratory reflexes (hyperventilation and sympathetic activation) triggered by hypoxia. The CB is composed of clusters of cells (glomeruli) in close contact with blood vessels and nerve fibers. Glomus cells, the O2-sensitive elements in the CB, are neuron-like cells that contain O2-sensitive K+ channels, which are inhibited by hypoxia. This leads to cell depolarization, Ca2+ entry, and the release of transmitters to activate sensory fibers terminating at the respiratory center. The mechanism whereby O2 modulates K+ channels has remained elusive, although several appealing hypotheses have been postulated. Recent data suggest that mitochondria complex I signaling to membrane K+ channels plays a fundamental role in acute O2 sensing. CB activation during exposure to low Po2 is also necessary for acclimatization to chronic hypoxia. CB growth during sustained hypoxia depends on the activation of a resident population of stem cells, which are also activated by transmitters released from the O2-sensitive glomus cells. These advances should foster further studies on the role of CB dysfunction in the pathogenesis of highly prevalent human diseases.

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