Article date: February 1996
By: Catherine Corriu, Michel Félétou, Emmanuel Canet, Paul M. Vanhoutte, in Volume 117, Issue 4, pages 607-610
Transmembrane potentials were recorded from isolated carotid arteries of the guinea‐pig superfused with modified Krebs‐Ringer bicarbonate solution. Smooth muscle cells were impaled with sharp intracellular microelectrodes.
Acetylcholine (I μm) induced an endothelium‐dependent hyperpolarization (14.3±2.8 mV, n=6) which was not affected (15.1±1.1 mV, n=35) by inhibitors of cyclo‐oxygenase (indomethacin, 5 μm) and nitric oxde synthase (Nωnitro‐L‐arginine: L‐NOARG, 100 μm).
The hyperpolarization produced by acetylcholine was abolished in the presence of elevated potassium (35 mM) in the superfusing physiological saline solution.
The acetylcholine‐induced hyperpolarization was not affected by the inhibitors of cytochrome P450 mono‐oxygenases, SKF525a (10 and 100 μm, 13.9±2.2 and 15.3±4.6 mV), metyrapone (100 μm, 13.1±1.9 mV), clotrimazole (100 μm, 13.5±2.7 mV), 17‐octadecynoic acid (5 μm 16.5±1.9 mV), methoxsalen (10 μm, 15.3±1.6 mV), the inhibitor of phospholipase A2 quinacrine (10 μm 12.8±2.5 mV) and the non specific lipoxygenases/cyclo‐oxygenases/cytochrome P450 inhibitor, eicosatetraynoic acid (50 μm, 15.0±2.2 mV). However, the muscarinic antagonist, atropine (100 nM), abolished the hyperpolarization.
These results suggest that in guinea‐pig carotid artery, the metabolism of arachidonic acid, either through cyclo‐oxygenase, lipoxygenase or cytochrome p450 mono‐oxygenase, is not involved in acetylcholine‐induced endothelium‐dependent hyperpolarizations.
Transmembrane potentials were recorded from isolated carotid arteries of the guinea‐pig superfused with modified Krebs‐Ringer bicarbonate solution. Smooth muscle cells were impaled with sharp intracellular microelectrodes.
Acetylcholine (I μm) induced an endothelium‐dependent hyperpolarization (14.3±2.8 mV, n=6) which was not affected (15.1±1.1 mV, n=35) by inhibitors of cyclo‐oxygenase (indomethacin, 5 μm) and nitric oxde synthase (Nωnitro‐L‐arginine: L‐NOARG, 100 μm).
The hyperpolarization produced by acetylcholine was abolished in the presence of elevated potassium (35 mM) in the superfusing physiological saline solution.
The acetylcholine‐induced hyperpolarization was not affected by the inhibitors of cytochrome P450 mono‐oxygenases, SKF525a (10 and 100 μm, 13.9±2.2 and 15.3±4.6 mV), metyrapone (100 μm, 13.1±1.9 mV), clotrimazole (100 μm, 13.5±2.7 mV), 17‐octadecynoic acid (5 μm 16.5±1.9 mV), methoxsalen (10 μm, 15.3±1.6 mV), the inhibitor of phospholipase A2 quinacrine (10 μm 12.8±2.5 mV) and the non specific lipoxygenases/cyclo‐oxygenases/cytochrome P450 inhibitor, eicosatetraynoic acid (50 μm, 15.0±2.2 mV). However, the muscarinic antagonist, atropine (100 nM), abolished the hyperpolarization.
These results suggest that in guinea‐pig carotid artery, the metabolism of arachidonic acid, either through cyclo‐oxygenase, lipoxygenase or cytochrome p450 mono‐oxygenase, is not involved in acetylcholine‐induced endothelium‐dependent hyperpolarizations.
DOI: 10.1111/j.1476-5381.1996.tb15233.x
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