fk-453 and fenamic-acid

fk-453 has been researched along with fenamic-acid* in 1 studies

Other Studies

1 other study(ies) available for fk-453 and fenamic-acid

Article	Year
Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein. Biochemical and biophysical research communications, 1994, Nov-15, Volume: 204, Issue:3 To examine the biological role of adenosine A1 receptors in bovine pulmonary artery endothelial cells, we measured intracellular Cl-concentration [Cl-]i, using 10mM 6-methoxy-N-(3-sulfopropyl) quinolinium monohydrate (SPQ). N6-cyclopentyladenosine (CPA), a selective A1 agonist, at 10(-8)M to 10(-5)M, rapidly decreased [Cl-]i by 30% to 51%, without a rapid elevation in [Ca2+]i and cyclic AMP. This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin (IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker). We conclude that an A1 receptor in endothelial cells activates Cl- efflux via a PTX-sensitive G protein. Topics: Adenosine; Animals; Calcium; Calcium Channel Blockers; Cattle; Cells, Cultured; Chlorides; Cyclic AMP; Dose-Response Relationship, Drug; Egtazic Acid; Endothelium, Vascular; GTP-Binding Proteins; Kinetics; ortho-Aminobenzoates; Pertussis Toxin; Pulmonary Artery; Purinergic Antagonists; Pyrazoles; Pyridines; Quinolinium Compounds; Spectrometry, Fluorescence; Virulence Factors, Bordetella	1994

Article

Year

Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein.

Biochemical and biophysical research communications, 1994, Nov-15, Volume: 204, Issue:3

To examine the biological role of adenosine A1 receptors in bovine pulmonary artery endothelial cells, we measured intracellular Cl-concentration [Cl-]i, using 10mM 6-methoxy-N-(3-sulfopropyl) quinolinium monohydrate (SPQ). N6-cyclopentyladenosine (CPA), a selective A1 agonist, at 10(-8)M to 10(-5)M, rapidly decreased [Cl-]i by 30% to 51%, without a rapid elevation in [Ca2+]i and cyclic AMP. This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin (IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker). We conclude that an A1 receptor in endothelial cells activates Cl- efflux via a PTX-sensitive G protein.

Topics: Adenosine; Animals; Calcium; Calcium Channel Blockers; Cattle; Cells, Cultured; Chlorides; Cyclic AMP; Dose-Response Relationship, Drug; Egtazic Acid; Endothelium, Vascular; GTP-Binding Proteins; Kinetics; ortho-Aminobenzoates; Pertussis Toxin; Pulmonary Artery; Purinergic Antagonists; Pyrazoles; Pyridines; Quinolinium Compounds; Spectrometry, Fluorescence; Virulence Factors, Bordetella

1994