Endothelin-triggered brain damage under hypoglycemia evidenced by real-time monitoring of dopamine release from rat striatal slices.
The role of endothelin in the pathogenesis of hypoglycemic brain damage in rats was evaluated using an in vitro model with which we could directly monitor the release of dopamine from striatal slices. There was no evidence of impairment in case of non-exposure of the slices to endothelin during 20-40 min of hypoglycemia. The response all but disappeared in striatal slices stimulated with endothelin 10(-5) M twice during 20 min of hypoglycemia. Endothelin-triggered hypoglycemic damage was not observed in the absence of extracellular Ca2+ or in the presence of nifedipine 10(-6) M. Our findings provide strong evidence that endothelin is one etiological factor in the development of hypoglycemic/ischemic brain injury, as a result of interaction with specific receptors which activate the voltage-sensitive Ca2+ channel.
Kataoka
Y
Y
Department of Pharmacology II Nagasaki University School of Medicine, Japan.
Koizumi
S
S
Kumakura
K
K
Kurihara
M
M
Niwa
M
M
Ueki
S
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001927:Brain Diseases / Q000378:metabolism* / Q000503:physiopathology; D003342:Corpus Striatum / Q000378:metabolism* / Q000503:physiopathology; D004298:Dopamine / Q000378:metabolism*; D016232:Endothelins; D007003:Hypoglycemia / Q000378:metabolism* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D010455:Peptides / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D016232:Endothelins; D010455:Peptides; D004298:Dopamine