Norepinephrine efflux evoked by potassium chloride in cat sympathetic nerves: dual mechanism of action.
Using a dialysis technique, prominent efflux of norepinephrine (NE) from cardiac sympathetic nerve endings was observed under local administration of potassium chloride (KCl, 100 mM). KCl induced NE efflux was suppressed by omega-conotoxin GVIA or desipramine but residual efflux of NE was still detectable. In the presence of omega-conotoxin GVIA, KCl induced efflux of NE was augmented by pretreatment with reserpine, indicating that this efflux of NE was derived from axoplasma with neurotransporter. These data suggest that a KCl induced brisk increase in dialysate NE levels might occur as a consequence of exocytotic NE release and carrier mediated outward NE transport from nerve endings.
Yamazaki
T
T
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565, Japan. yamazaki@ri.ncvc.go.jp
Akiyama
T
T
Kawada
T
T
Kitagawa
H
H
Takauchi
Y
Y
Yahagi
N
N
Sunagawa
K
K
D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000818:Animals; D002415:Cats; D003891:Desipramine / Q000494:pharmacology; D004357:Drug Synergism; D005089:Exocytosis / Q000187:drug effects*; D005260:Female; D008297:Male; D009411:Nerve Endings / Q000187:drug effects* / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology*; D012110:Reserpine / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000378:metabolism; D020866:omega-Conotoxin GVIA
D018759:Adrenergic Uptake Inhibitors; D010455:Peptides; D011189:Potassium Chloride; D012110:Reserpine; D020866:omega-Conotoxin GVIA; D003891:Desipramine; D009638:Norepinephrine