Na+ channel block prevents the ischemia-induced release of norepinephrine from spinal cord slices
Autor: | Tetsuo Sato, E. Sylvester Vizi, Tetsuji Nakai, Agnes Bencsics, Eiichiro Umeda, Yoshitaka Uchihashi |
---|---|
Rok vydání: | 1998 |
Předmět: |
Male
Sodium Ischemia chemistry.chemical_element Tetrodotoxin Pharmacology Rats Sprague-Dawley Norepinephrine chemistry.chemical_compound Sodium channel blocker medicine Animals 4-Aminopyridine Anesthetics Local Hypoxia business.industry Lidocaine Hypoxia (medical) Calcium Channel Blockers medicine.disease Spinal cord Hypoglycemia Pathophysiology Rats Cold Temperature medicine.anatomical_structure Spinal Cord chemistry Anesthesia Catecholamine Calcium medicine.symptom business Sodium Channel Blockers medicine.drug |
Zdroj: | European Journal of Pharmacology. 346:145-150 |
ISSN: | 0014-2999 |
DOI: | 10.1016/s0014-2999(98)00049-1 |
Popis: | The principal finding of the present study with rat spinal cord slices was the novel demonstration of the [Ca2+]o-independent effect of ischemia on norepinephrine release and its antagonism by tetrodotoxin and low temperature (10 degrees C). Our finding that tetrodotoxin antagonized the effects of glucose deprivation on norepinephrine release in a [Ca2+]o-independent way suggests that Na+ channel block alone, i.e., the prevention of Na+ accumulation, may account for the protective action. Low temperature completely prevented the effect of ischemia on norepinephrine release but did not change the release associated with axonal activity. This finding is in good agreement with the observation that small changes in brain temperature critically determine the extent of neuronal injury from ischemia and suggests that both [Ca2+]o-independent release and cell injury are associated with the norepinephrine membrane carrier. It is suggested, therefore, that drugs able to attenuate the increase in [Na+]i during ischemia may be useful agents to protect against ischemic damage if given before the insult. |
Databáze: | OpenAIRE |
Externí odkaz: |