Stimulation of Prostacyclin Production from Vascular Endothelial Cells by Factors Present in Plasma, Serum and Platelets

1981 ◽  
Vol 61 (3) ◽  
pp. 22P-23P
Author(s):  
J.M. Seid ◽  
P.B.B. Jones ◽  
R.G.G. Russell
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Prostacyclin Production ◽  
Stimulation Of

Human serum stimulates endothelin-1 synthesis more potently than prostacyclin production by cultured vascular endothelial cells

Life Sciences ◽  
1991 ◽  
Vol 49 (8) ◽  
pp. 603-609 ◽  
Author(s):  
Ari Ristimäki ◽  
Risto Renkonen ◽  
Outi Saijonmaa ◽  
Olavi Ylikorkala ◽  
Lasse Viinikka
Keyword(s):  
Endothelial Cells ◽  
Human Serum ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
Prostacyclin Production

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 ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cyclic Gmp ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Prostacyclin Production

Effects of Homocysteine and Related Compounds on Prostacyclin Production by Cultured Human Vascular Endothelial Cells

1993 ◽  
Vol 70 (06) ◽  
pp. 1047-1052 ◽  
Author(s):  
Jian Wang ◽  
Nicholas P B Dudman ◽  
David E L Wilcken
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Calf Serum ◽  
Consistent Difference ◽  
Vascular Endothelial ◽  
Intravascular Thrombosis ◽  
Increased Risk ◽  
Related Compounds ◽  
Prostacyclin Production ◽  
Cells Cultured

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.

Prostacyclin: Production by Vascular Endothelium and Effects on Platelet Aggregation

1979 ◽  
Author(s):  
S. Moncada ◽  
S. Bunting
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Vascular Endothelium ◽  
Vascular Endothelial Cells ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Prostacyclin Production

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.

scholarly journals Human Vascular Endothelial Cells Express Oxytocin Receptors*

Endocrinology ◽  
1999 ◽  
Vol 140 (3) ◽  
pp. 1301-1309 ◽  
Author(s):  
Marc Thibonnier ◽  
Doreen M. Conarty ◽  
Judy A. Preston ◽  
Christine L. Plesnicher ◽  
Raed A. Dweik ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Intracellular Calcium ◽  
Vascular Endothelial Cells ◽  
Primary Cultures ◽  
Receptor Subtype ◽  
Vascular Endothelial ◽  
Degenerate Primers ◽  
Vasodilatory Response ◽  
Stimulation Of

Abstract Pharmacological studies in humans and animals suggest the existence of vascular endothelial vasopressin (AVP)/oxytocin (OT) receptors that mediate a vasodilatory effect. However, the nature of the receptor subtype(s) involved in this vasodilatory response remains controversial, and its coupled intracellular pathways are unknown. Thus, we set out to determine the type and signaling pathways of the AVP/OT receptor(s) expressed in human vascular endothelial cells (ECs). Saturation binding experiments with purified membranes of primary cultures of ECs from human umbilical vein (HUVEC), aorta (HAEC), and pulmonary artery (HPAEC) and [3H]AVP or[ 3H]OT revealed the existence of specific binding sites with a greater affinity for OT than AVP (Kd = 1.75 vs. 16.58 nm). Competition binding experiments in intact HUVECs (ECV304 cell line) with the AVP antagonist[ 125I]4-hydroxyphenacetyl-d-Tyr(Me)-Phe-Gln-Asn-Arg-Pro-Arg-NH2 or the OT antagonist[ 125I]d(CH2)5[O-Me-Tyr-Thr-Orn-Tyr-NH2]vasotocin, and various AVP/OT analogs confirmed the existence of a single class of surface receptors of the classical OT subtype. RT-PCR experiments with total RNA extracted from HUVEC, HAEC, and HPAEC and specific primers for the human V1 vascular, V2 renal, V3 pituitary, and OT receptors amplified the OT receptor sequence only. No new receptor subtype could be amplified when using degenerate primers. DNA sequencing of the coding region of the human EC OT receptor revealed a nucleotide sequence 100% homologous to that of the uterine OT receptor reported previously. Stimulation of ECs by OT produced mobilization of intracellular calcium and the release of nitric oxide that was prevented by chelation of extra- and intracellular calcium. No stimulation of cAMP or PG production was noted. Finally, OT stimulation of ECs led to a calcium- and protein kinase C-dependent cellular proliferation response. Thus, human vascular ECs express OT receptors that are structurally identical to the uterine and mammary OT receptors. These endothelial OT receptors produce a calcium-dependent vasodilatory response via stimulation of the nitric oxide pathway and have a trophic action.

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