scholarly journals Hypoxic pulmonary vasoconstriction: role of voltage-gated potassium channels

10.1186/rr11 ◽  
2000 ◽  
Vol 1 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Michèle Sweeney ◽  
Jason X-J Yuan
Keyword(s):  
Potassium Channels ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Voltage Gated ◽  
Pulmonary Vasoconstriction

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)

scholarly journals Evidence for a role of protein kinase C in hypoxic pulmonary vasoconstriction

1999 ◽  
Vol 276 (1) ◽  
pp. L90-L95 ◽  
Author(s):  
Norbert Weissmann ◽  
Robert Voswinckel ◽  
Thorsten Hardebusch ◽  
Simone Rosseau ◽  
Hossein Ardeschir Ghofrani ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Ang Ii ◽  
Pkc Inhibitor ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction

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 signaling response to hypoxia. Because protein kinase (PK) C activation can occur during hypoxia and PKC activation is known to be critical for NADPH oxidase stimulation in different cell types, we probed the role of PKC in hypoxic vasoconstriction in intact rabbit lungs. Control vasoconstrictor responses were elicited by angiotensin II (ANG II) and the stable thromboxane analog U-46619. Portions of the experiments were performed while NO synthesis and prostanoid generation were blocked with N G-monomethyl-l-arginine and acetylsalicylic acid to avoid confounding effects due to interference with these vasoactive mediators. The PKC inhibitor H-7 (10–50 μM) caused dose-dependent inhibition of HPV, but this agent lacked specificity because ANG II- and U-46619-induced vasoconstrictions were correspondingly suppressed. In contrast, low concentrations of the specific PKC inhibitor bisindolylmaleimide I (BIM; 1–15 μM) strongly inhibited the hypoxic vasoconstriction without any interference with the responses to the pharmacological agents. Superimposable dose-inhibition curves were also obtained for BIM when lung NO synthesis and prostanoid generation were blocked throughout the experiments. Under either condition, BIM did not affect normoxic vascular tone. The PKC activator farnesylthiotriazole (FTT), ascertained to stimulate rabbit NADPH oxidase by provocation of alveolar macrophage superoxide anion generation in vitro, caused rapid-onset, transient pressor responses in normoxic lungs. After FTT, the hypoxic vasoconstrictor response was totally suppressed, in contrast to the largely maintained pressor responses to ANG II and U-46619. The lungs became refractory even to delayed hypoxic challenges after FTT application. In conclusion, these data support the concept that activation of PKC is involved in the transduction pathway forwarding pulmonary vasoconstriction in response to alveolar hypoxia.

Prostaglandin synthesis inhibition restores hypoxic pulmonary vasoconstriction

1977 ◽  
Vol 42 (6) ◽  
pp. 903-908 ◽  
Author(s):  
J. M. Alexander ◽  
M. D. Nyby ◽  
K. A. Jasberg
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Prostaglandin Synthesis ◽  
Hypoxic Response ◽  
Synthesis Inhibition ◽  
Pulmonary Vasoconstriction ◽  
Isolated Lungs ◽  
The Right

Hypoxic pulmonary vasoconstriction in blood-perfused isolated dog lungs progressively diminishes with repeated hypoxic challenges. We investigated the role of prostaglandins in effecting the decay of the hypoxic response by using a double perfusion preparation that could separately perfuse the right and left lungs of a single dog. Degeneration of this response was reversed by the addition of prostaglandin (PG) synthesis inhibitors, aspirin, or indomethacin. Various PG's known to be produced by the lung (PGE1, PGE2, and PGF2alpha), were infused, and only PGE1 abolished hypoxic pulmonary vasoconstriction. Since other workers have shown that lungs can synthesize and release PG's in response to various stimuli, we postulate that PGE1 synthesis in isolated lungs may increase and thereby cause the degeneration of the hypoxic response. The addition of aspirin or indomethacin could inhibit the synthesis of PGE1 and thereby restore hypoxic pulmonary vasoconstriction.

Role of protein kinase C in 15-HETE-induced hypoxic pulmonary vasoconstriction

2009 ◽  
Vol 80 (2-3) ◽  
pp. 115-123 ◽  
Author(s):  
Lei Guo ◽  
Xiaobo Tang ◽  
Xiaojie Chu ◽  
Lihua Sun ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction ◽  
Kinase C
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