Effect of celecoxib on cyclooxygenase-1-mediated prostacyclin synthesis and endothelium-dependent contraction in mouse arteries

2013 ◽  
Vol 698 (1-3) ◽  
pp. 354-361 ◽  
Author(s):  
Bin Liu ◽  
Wenhong Luo ◽  
Yingzhan Zhang ◽  
Hui Li ◽  
Ningxia Zhu ◽  
...  
Keyword(s):  
Cyclooxygenase 1 ◽  
Prostacyclin Synthesis

scholarly journals Vasomotor Reaction to Cyclooxygenase-1-Mediated Prostacyclin Synthesis in Carotid Arteries from Two-Kidney-One-Clip Hypertensive Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136738 ◽  
Author(s):  
Bin Liu ◽  
Zhenhua Li ◽  
Yingzhan Zhang ◽  
Wenhong Luo ◽  
Jiling Zhang ◽  
...  
Keyword(s):  
Carotid Arteries ◽  
Vasomotor Reaction ◽  
Cyclooxygenase 1 ◽  
Prostacyclin Synthesis

scholarly journals Hypoxia stimulates prostacyclin synthesis in newborn pulmonary artery endothelium by increasing cyclooxygenase-1 protein.

1994 ◽  
Vol 75 (1) ◽  
pp. 33-40 ◽  
Author(s):  
A J North ◽  
T S Brannon ◽  
L B Wells ◽  
W B Campbell ◽  
P W Shaul
Keyword(s):  
Pulmonary Artery ◽  
Cyclooxygenase 1 ◽  
Prostacyclin Synthesis

Prostacyclin Synthesis Is Stimulated by a Serum Factor Formed During Coagulation

1983 ◽  
Vol 49 (01) ◽  
pp. 058-060 ◽  
Author(s):  
J M Ritter ◽  
M-A Ongari ◽  
M A Orchard ◽  
P J Lewis
Keyword(s):  
Renal Failure ◽  
Hydrolysis Product ◽  
Healthy Controls ◽  
Serum Factor ◽  
Intrinsic Pathway ◽  
Extrinsic Pathway ◽  
Stimulatory Activity ◽  
Plasma Factor ◽  
Stimulating Factor ◽  
Prostacyclin Synthesis

SummaryFresh aortic rings incubated in serum produce more 6-oxo-PGF1α, the stable hydrolysis product of prostacyclin, than in plasma or buffer. A method is described of recovering this stimulatory activity from a dialysate of serum, showing that the activity is due to a prostacyclin stimulating factor. This factor is formed during coagulation initiated by the intrinsic pathway but not by the extrinsic pathway or by thrombin. By contrast with a previously described plasma factor, the activity of the prostacy-clinstimulating factor in serum is not greater in serum from patients with renal failure than from healthy controls. The stimulating factor is antagonised by heparin, but differs in other ways from previously described platelet derived stimulating factor(s).

Effects of Aspirin and Sulfinpyrazone on Thromboxane and Prostacyclin Synthesis in Rabbits

1979 ◽  
Author(s):  
J McDonald ◽  
A Cerskus ◽  
M Ali
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Low Dose ◽  
High Dose ◽  
Prostacyclin Synthesis

Arachidonic acid (AA) or collagen were infused into rabbits causing intravascular platelet aggregation with thrombocytopenia, hypotension and death. Thromboxane and prostacyclin synthesis were measured by radioimmunoassay of plasma TXB2 and 6-keto-PGF1α. The effects of pretreatement with aspirin (ASA) or sulfinpyrazone(SPZ) were assessed.Death in drug-treated rabbits was always associated with elevations of plasma TXB2(1-40 ng/ml) and of 6-keto-PGF1α(1-20 ng/ml). Collagen produced only small elevations of plasma TXB2 compared to AA but protection by ASA correlated better with inhibition of TXB2 and 6-keto-PGF1α synthesis than with inhibition of aggregation. Low dose ASA produced less inhibition of prostacyclin synthesis than high dose ASA but was less effective in preventing thromboxane synthesis and death.

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