scholarly journals Dexamethasone induces rapid promotion of norepinephrine-mediated vascular smooth muscle cell contraction

2012 ◽  
Vol 7 (2) ◽  
pp. 549-554 ◽  
Author(s):  
TING ZHANG ◽  
WEN-LEI SHI ◽  
JEFFREY G. TASKER ◽  
JIANG-RUI ZHOU ◽  
YUN-LI PENG ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Contraction

Ticagrelor, but not clopidogrel and prasugrel, prevents ADP-induced vascular smooth muscle cell contraction: A placebo-controlled study in rats

2012 ◽  
Vol 130 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Grzegorz Grzesk ◽  
Marek Kozinski ◽  
Eliano Pio Navarese ◽  
Marek Krzyzanowski ◽  
Elzbieta Grzesk ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Controlled Study ◽  
Cell Contraction

scholarly journals Vascular smooth muscle cell contraction and relaxation in the isolated aorta: a critical regulator of large artery compliance

2019 ◽  
Vol 7 (4) ◽  
pp. e13934 ◽  
Author(s):  
Arthur J. A. Leloup ◽  
Cor E. Van Hove ◽  
Sofie De Moudt ◽  
Guido R. Y. De Meyer ◽  
Gilles W. De Keulenaer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Large Artery ◽  
Cell Contraction ◽  
Isolated Aorta ◽  
Contraction And Relaxation

scholarly journals Role for G 12 /G 13 in Agonist-Induced Vascular Smooth Muscle Cell Contraction

2000 ◽  
Vol 87 (3) ◽  
pp. 221-227 ◽  
Author(s):  
Antje Gohla ◽  
Günter Schultz ◽  
Stefan Offermanns
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Contraction ◽  
G 12 ◽  
G 13

Involvement of Cyclooxygenase- and Lipoxygenase-Mediated Conversion of Arachidonic Acid in Controlling Human Vascular Smooth Muscle Cell Proliferation

1990 ◽  
Vol 63 (02) ◽  
pp. 291-297 ◽  
Author(s):  
Herm-Jan M Brinkman ◽  
Marijke F van Buul-Worteiboer ◽  
Jan A van Mourik
Keyword(s):  
Cell Proliferation ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Muscle Cells ◽  
Smooth Muscle Cell Proliferation

SummaryWe observed that the growth of human umbilical arterysmooth muscle cells was inhibited by the phospholipase A2 inhibitors p-bromophenacylbromide and mepacrine. Thesefindings suggest that fatty acid metabolism might be integrated in the control mechanism of vascular smooth muscle cell proliferation. To identify eicosanoids possibly involved in this process, we studied both the metabolism of arachidonic acid of these cells in more detail and the effect of certain arachidonic acid metabolites on smooth muscle cells growth. We found no evidence for the conversion of arachidonic acid via the lipoxygenase pathway. In contrast, arachidonic acid was rapidly converted via the cyclooxy-genase pathway. The following metabolites were identified: prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-k-PGF1α), prostaglandin F2α (PGF2α), 12-hydroxyheptadecatrienoic acid (12-HHT) and 11-hydroxyeicosatetetraenoic acid (11-HETE). PGE2 was the major metabolite detected. Arachidonic acid metabolites were only found in the culture medium, not in the cell. After synthesis, 11-HETE was cleared from the culture medium. We have previously reported that PGE2 inhibits the serum-induced [3H]-thymidine incorporation of growth-arrested human umbilical artery smooth muscle cells. Here we show that also 11-HETEexerts this inhibitory property. Thus, our data suggeststhat human umbilical artery smooth muscle cells convert arachidonic acid only via the cyclooxygenase pathway. Certain metabolites produced by this pathway, including PGE2 and 11-HETE, may inhibit vascular smooth muscle cell proliferation.

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