Possible involvement of amino acid transporters on S-nitroso-cysteine-induced inhibition of arachidonic acid release in PC12 cells

2001 ◽  
Vol 311 (2) ◽  
pp. 117-120 ◽  
Author(s):  
Takanori Nemoto ◽  
Syunji Horie ◽  
Yasunobu Okuma ◽  
Yasuyuki Nomura ◽  
Toshihiko Murayama
Keyword(s):  
Arachidonic Acid ◽  
Amino Acid ◽  
Pc12 Cells ◽  
Amino Acid Transporters ◽  
Arachidonic Acid Release ◽  
Acid Release

scholarly journals ATP receptor-mediated arachidonic acid release from PC12 cells.

1994 ◽  
Vol 64 ◽  
pp. 322
Author(s):  
Toshihiko Murayama ◽  
Asako Watanabe ◽  
Yasuyuki Nomura
Keyword(s):  
Arachidonic Acid ◽  
Pc12 Cells ◽  
Arachidonic Acid Release ◽  
Acid Release

Pharmacology of endothelin receptor antagonists ABT-627, ABT-546, A-182086 and A-192621: in vitro studies

2002 ◽  
Vol 103 (s2002) ◽  
pp. 107S-111S ◽  
Author(s):  
J. Ruth WU-WONG ◽  
Douglas B. DIXON ◽  
William J. CHIOU ◽  
Brian K. SORENSEN ◽  
Gang LIU ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Amino Acid ◽  
Small Molecule ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Arachidonic Acid Release ◽  
Functional Responses ◽  
Receptor Antagonists ◽  
Acid Release

Endothelins (ETs), 21-amino-acid peptides involved in the pathogenesis of various diseases, bind to ETA and ETB receptors to initiate their effects. Based on the same core structure, we have developed four small-molecule ET receptor antagonists, ABT-627, ABT-546, A-182086 and A-192621, which exhibit difference in selectivity for ETA and ETB receptors. In this report, we compare the potency and selectivity of these four antagonists in inhibiting 125I-labelled ET-1 binding to cloned human ETA and ETB receptors, and in blocking ET-1-induced functional responses (arachidonic acid release and phosphatidylinositol hydrolysis).

PGE2 release by bradykinin in human airway smooth muscle cells: involvement of cyclooxygenase-2 induction

1997 ◽  
Vol 273 (6) ◽  
pp. L1132-L1140 ◽  
Author(s):  
Linhua Pang ◽  
Alan J. Knox
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Arachidonic Acid Release ◽  
Human Airway Smooth Muscle ◽  
Short Term ◽  
Human Airway ◽  
Acid Release ◽  
Cox 2

Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma. We investigated whether cyclooxygenase (COX)-2 induction was involved in prostaglandin (PG) E2 release by BK in cultured human airway smooth muscle (ASM) cells and analyzed the BK receptor subtypes responsible. BK stimulated PGE2release, COX activity, and COX-2 induction in a concentration- and time-dependent manner. It also time dependently enhanced arachidonic acid release. In short-term (15-min) experiments, BK stimulated PGE2 generation but did not increase COX activity or induce COX-2. In long-term (4-h) experiments, BK enhanced PGE2 release and COX activity and induced COX-2. The long-term responses were inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and the steroid dexamethasone. The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations. The B2antagonist HOE-140 potently inhibited all the effects, but the B1 antagonist des-Arg9,(Leu8)-BK was inactive. This study is the first to demonstrate that BK can induce COX-2. Conversion of increased arachidonic acid release to PGE2 by COX-1 is mainly involved in the short-term effect, whereas B2 receptor-related COX-2 induction is important in the long-term PGE2 release.

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