흰쥐 대뇌피질 절편에서 허혈에 의한 Norepinephrine 유리에 있어서 Nitric Oxide의 영향

• 영문명: Role of Nitric Oxide in Ischemia-evoked Release of Norepinephrine from Rat Cortex Slices
• 발행기관: 대한생리학회-대한약리학회
• 저자명: 김기원(Kee Won Kim) 은영아(Young Ah Eun) 김동찬(Dong Chan Kim) 조규박(Kyu Park Cho)
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제1권 제6호, 673~679쪽, 전체 7쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 1997.01.01

영문 초록

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced [³H]norepinephrine([³H]NE) release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from Mg^2⁢-free artificial cerebrospinal fluid, induced significant release of [³H]NE from cortex slices. This ischemia-induced [³H]NE release was significantly attenuated by glutamatergic neurotransmission modifiers. N^G-nitro-L-arginine methyl ester(L-NAME), N^G-monomethyl-L-arginine (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked [³H]NE release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited [³H]NE release dose-dependently. Ischemia-evoked [³H]NE release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked [³H]NE release is mediated by NMDA receptors, and activation of NO system is involved.

키워드

Cerebral ischemia Norepinephrine release Nitric Oside