scholarly journals Effect of cyclic GMP and sulfhydryl on prostacyclin production by human vascular endothelial cells.

1991 ◽  
Vol 55 (6) ◽  
pp. 643-647 ◽  
Author(s):  
KYOCHIRO KOBAYASHI ◽  
TAKEO TOYODA ◽  
SYOHEI SAWADA ◽  
KAORU SHIRAI ◽  
KATSUMI YAMAMOTO ◽  
...  
Life Sciences ◽  
1991 ◽  
Vol 49 (8) ◽  
pp. 603-609 ◽  
Author(s):  
Ari Ristimäki ◽  
Risto Renkonen ◽  
Outi Saijonmaa ◽  
Olavi Ylikorkala ◽  
Lasse Viinikka

2003 ◽  
Vol 66 (2) ◽  
pp. 263-271 ◽  
Author(s):  
Hun-Kung Hsu ◽  
Shu-Hui Juan ◽  
Pei-Yin Ho ◽  
Yu-Chih Liang ◽  
Chien-Huang Lin ◽  
...  

1989 ◽  
Vol 20 (6) ◽  
pp. 545-552
Author(s):  
Kyoichiro KOBAYASHI ◽  
Takeo TOYODA ◽  
Syohei SAWADA ◽  
Kaoru SHIRAI ◽  
Katsumi YAMAMOTO ◽  
...  

1993 ◽  
Vol 70 (06) ◽  
pp. 1047-1052 ◽  
Author(s):  
Jian Wang ◽  
Nicholas P B Dudman ◽  
David E L Wilcken

SummaryElevated plasma homocysteine is associated with an increased risk of intravascular thrombosis. Platelet aggregation and thrombosis are inhibited by prostacyclin produced by the vascular endothelium. Our aim was to investigate whether homocysteine and related metabolites inhibit endothelial prostacyclin production. We used a radioimmunoassay for 6-ketoprostaglandin-F1α to assay medium which had been in contact with confluent cultured endothelial cells. In medium containing 20% human serum, endothelial prostacyclin production was not specifically inhibited by homocysteine, S-adenosylhomocysteine or protein-bound homocysteine. Further, there was no consistent difference in prostacyclin production by cells cultured in medium containing sera from homocystinuria patients, compared with medium containing normal healthy sera. We conclude that vascular disorder in homocystinuria is unlikely to result from effects of homocysteine or related metabolites on endothelial prostacyclin production. By contrast, S-adenosylhomocysteine and protein-bound homocysteine specifically inhibited prostacyclin production by cells cultured in medium containing 20% fetal calf serum.


1979 ◽  
Author(s):  
S. Moncada ◽  
S. Bunting

The inhibitory effect of vascular endothelial cells on platelet aggregation is due to their ability to release prostacyclin. The existence of an ADPase has been confirmed in endothelial cells but this enzymes does not seem to be related to the anti-aggregating properties of vascular endothelium. In vitro, the release of prostacyclin by humand and rabbit endothelial cells persists after several subcultures. The production of PGI2 can be demonstrated by its inhibition by aspirin-like drugs or 15-hydroperoxy arachidonic acid (a specific inhibitor of PGI2 synthesis). Moreover, the antiaggregating activity is antagonised by an antibody to 5,6 dihydro prostacyclin which cross reacts and neutralises prostacyclin.


1991 ◽  
Vol 72 (3) ◽  
pp. 623-627 ◽  
Author(s):  
ARI RISTIMÄKI ◽  
OLAVI YLIKORKALA ◽  
KRISTINA PESONEN ◽  
JAAKKO PERHEENTUPA ◽  
LASSE VIINIKKA

1984 ◽  
Vol 73 (1) ◽  
pp. 251-257 ◽  
Author(s):  
A Eldor ◽  
R Fridman ◽  
I Vlodavsky ◽  
E Hy-Am ◽  
Z Fuks ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document