scholarly journals Ceramide and Regulation of Vascular Tone

2019 ◽  
Vol 20 (2) ◽  
pp. 411 ◽  
Author(s):  
Angel Cogolludo ◽  
Eduardo Villamor ◽  
Francisco Perez-Vizcaino ◽  
Laura Moreno
Keyword(s):  
Lung Diseases ◽  
Vascular Tone ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Ductus Arteriosus ◽  
Complex Interaction ◽  
Oxygen Species ◽  
Pulmonary Vasoconstriction ◽  
Physiological Relevance ◽  
Regulation Of Vascular Tone

In addition to playing a role as a structural component of cellular membranes, ceramide is now clearly recognized as a bioactive lipid implicated in a variety of physiological functions. This review aims to provide updated information on the role of ceramide in the regulation of vascular tone. Ceramide may induce vasodilator or vasoconstrictor effects by interacting with several signaling pathways in endothelial and smooth muscle cells. There is a clear, albeit complex, interaction between ceramide and redox signaling. In fact, reactive oxygen species (ROS) activate different ceramide generating pathways and, conversely, ceramide is known to increase ROS production. In recent years, ceramide has emerged as a novel key player in oxygen sensing in vascular cells and mediating vascular responses of crucial physiological relevance such as hypoxic pulmonary vasoconstriction (HPV) or normoxic ductus arteriosus constriction. Likewise, a growing body of evidence over the last years suggests that exaggerated production of vascular ceramide may have detrimental effects in a number of pathological processes including cardiovascular and lung diseases.

scholarly journals Hypoxic Pulmonary Vasoconstriction in Humans: Tale or Myth

2017 ◽  
Vol 11 (1) ◽  
pp. 1-13 ◽  
Author(s):  
A. Hussain ◽  
M.S. Suleiman ◽  
S.J. George ◽  
M. Loubani ◽  
A. Morice
Keyword(s):  
Reactive Oxygen Species ◽  
Rho Gtpases ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Underlying Mechanism ◽  
Clinical Implications ◽  
Oxygen Species ◽  
Adaptive Process ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction

Hypoxic Pulmonary vasoconstriction (HPV) describes the physiological adaptive process of lungs to preserves systemic oxygenation. It has clinical implications in the development of pulmonary hypertension which impacts on outcomes of patients undergoing cardiothoracic surgery. This review examines both acute and chronic hypoxic vasoconstriction focusing on the distinct clinical implications and highlights the role of calcium and mitochondria in acute versus the role of reactive oxygen species and Rho GTPases in chronic HPV. Furthermore it identifies gaps of knowledge and need for further research in humans to clearly define this phenomenon and the underlying mechanism.

Vascular adaptations to hypoxia: molecular and cellular mechanisms regulating vascular tone

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker
Keyword(s):  
Vascular Tone ◽  
Cellular Proliferation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxia Inducible Factor ◽  
Systemic Circulation ◽  
Cellular Mechanisms ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Vasoconstriction ◽  
Adaptive Mechanisms ◽  
Adaptive Processes

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.

scholarly journals NADPH oxidase-derived ROS and the regulation of pulmonary vessel tone

2012 ◽  
Vol 302 (11) ◽  
pp. H2166-H2177 ◽  
Author(s):  
G. Frazziano ◽  
H. C. Champion ◽  
P. J. Pagano
Keyword(s):  
Oxygen Tension ◽  
Vascular Tone ◽  
Systemic Circulation ◽  
Oxygen Species ◽  
Partial Pressure Of Oxygen ◽  
Low Oxygen ◽  
Key Factors ◽  
Pulmonary Vessel ◽  
Major Emphasis

Pulmonary vessel constriction results from an imbalance between vasodilator and vasoconstrictor factors released by the endothelium including nitric oxide, endothelin, prostanoids, and reactive oxygen species (ROS). ROS, generated by a variety of enzymatic sources (such as mitochondria and NADPH oxidases, a.k.a. Nox), appear to play a pivotal role in vascular homeostasis, whereas elevated levels effect vascular disease. The pulmonary circulation is very sensitive to changes in the partial pressure of oxygen and differs from the systemic circulation in its response to this change. In fact, the pulmonary vessels contract in response to low oxygen tension, whereas systemic vessels dilate. Growing evidence suggests that ROS production and ROS-related pathways may be key factors that underlie this differential response to oxygen tension. A major emphasis of our laboratory is the role of Nox isozymes in cardiovascular disease. In this review, we will focus our attention on the role of Nox-derived ROS in the control of pulmonary vascular tone.

scholarly journals Recent advances in oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

2017 ◽  
Vol 123 (6) ◽  
pp. 1647-1656 ◽  
Author(s):  
Ievgen Strielkov ◽  
Oleg Pak ◽  
Natasha Sommer ◽  
Norbert Weissmann
Keyword(s):  
Reactive Oxygen Species ◽  
Transient Receptor Potential ◽  
Oxygen Sensing ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Reactive Oxygen ◽  
Receptor Potential ◽  
Complex Iii ◽  
Oxygen Species ◽  
Pulmonary Vasoconstriction ◽  
Transient Receptor

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, while generalized HPV contributes to the development of pulmonary hypertension. The triggering mechanisms underlying HPV are still not fully elucidated. Several hypotheses are currently under debate, including a possible decrease as well as an increase in reactive oxygen species as a triggering event. Recent findings suggest an increase in the production of reactive oxygen species in pulmonary artery smooth muscle cells by complex III of the mitochondrial electron transport chain and occurrence of oxygen sensing at complex IV. Other essential components are voltage-dependent potassium and possibly L-type, transient receptor potential channel 6, and transient receptor potential vanilloid 4 channels. The release of arachidonic acid metabolites appears also to be involved in HPV regulation. Further investigation of the HPV mechanisms will facilitate the development of novel therapeutic strategies for the treatment of HPV-related disorders.

scholarly journals Role of ATP-sensitive potassium channels on hypoxic pulmonary vasoconstriction in endotoxemia

2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Maurizio Turzo ◽  
Julian Vaith ◽  
Felix Lasitschka ◽  
Markus A. Weigand ◽  
Cornelius J. Busch
Keyword(s):  
Potassium Channels ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

Endothelium-derived relaxing factor activity in rat lung during hypoxic pulmonary vascular remodeling

1993 ◽  
Vol 74 (3) ◽  
pp. 1061-1065 ◽  
Author(s):  
L. Zhao ◽  
D. E. Crawley ◽  
J. M. Hughes ◽  
T. W. Evans ◽  
R. J. Winter
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxic Exposure ◽  
Control Group ◽  
Pulmonary Vascular Remodeling ◽  
Relaxing Factor ◽  
Pulmonary Vasoconstriction ◽  
O2 Concentration ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

We have investigated the role of endothelium-derived relaxing factor in modulating hypoxic pulmonary vasoconstriction by inhibiting its synthesis with the false substrate NG-monomethyl-L-arginine (L-NMMA) in the isolated blood-perfused lungs of Wistar rats after chronic hypoxia (CH, fractional inspiratory O2 concentration 10%) for 15 h, 2 days, and 7 days. Lungs were perfused with blood of normal hematocrit at constant flow (18 ml/min) ventilated with 1) 95% air-5% CO2 (normoxia) and 2) 2% O2–5% CO2-93% N2 (hypoxia) and were studied in the absence and presence of L-NMMA (30 and 300 microM) or L-arginine (L-Arg, 1 and 6 mM) in separate groups. Pulmonary arterial pressure (Ppa) rose incrementally with hypoxic exposure (all P < 0.05 vs. normoxic control group). Hypoxic pulmonary vasoconstriction (HPV) was markedly reduced after 15 h and 2 days of CH: the mean increases in Ppa (delta Ppa) in hypoxia were 15.3, 3.5, 3.8, and 13.6 mmHg in control rats and rats exposed to 15 h (P < 0.05 vs. control and 7 days of CH), 2 days (P < 0.001 vs. control and 7 days of CH), and 7 days of CH, respectively. Ppa in control rats and rats exposed to 15 h, 2 days, and 7 days of CH were 137, 179, 184, and 166% of control, respectively, after 30 microM L-NMMA (all P < 0.05 when expressed as percent change vs. no L-NMMA). Similar augmentation in HPV was seen after 30 microM L-NMMA, with all hypoxic groups having a greater response than control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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