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Neuroprotective effects of carvedilol, a new antihypertensive, at the N-methyl-D-aspartate receptor.

Abstract：

:Carvedilol's potent antioxidant activity could explain its protective action in brain ischemia, but may not apply to glutamate-induced excitotoxicity in cultured cerebellar granule cells, since glutamate neurotoxicity was not associated with the formation of lipid peroxidative products. Rather, carvedilol diminished the N-methyl-D-aspartate (NMDA)/glycine-induced increase in intracellular calcium ([Ca2+]i), lowering [Ca2+]i by a maximum of 66 +/- 5% (n = 8) with a 50% inhibitory concentration of 0.8 microM. Prior addition of 5 microM dihydropyridines did not shift the dose-response of carvedilol, but did significantly lower the NMDA/glycine-stimulated response to 64% of untreated (n = 8, P = 0.014). Inclusion of 5 microM carvedilol before the additions of NMDA/glycine prevented 85% of the increase in [Ca2+]i. Furthermore, carvedilol displaced 3[H]MK-801 binding to rat brain cortical membranes with a Kd of 29.4 +/- 2.2 microM (n = 6) and no selectively for the glutamate or glycine binding sites. These data therefore suggest that, in addition to its antihypertensive and anti-lipid peroxidative functions, carvedilol has neuroprotective activity as a calcium channel blocker and as a non-competitive inhibitor at the NMDA receptor.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Lysko PG,Lysko KA,Webb CL,Feuerstein G

doi

10.1016/0304-3940(92)90798-c

keywords:

subject

Has Abstract

pub_date

1992-12-14 00:00:00

pages

34-8

issue

1-2

eissn

0304-3940

issn

1872-7972

pii

0304-3940(92)90798-C

journal_volume

148

pub_type

杂志文章

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