期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 623, 期 1-3, 页码 113-118出版社
ELSEVIER
DOI: 10.1016/j.ejphar.2009.09.023
关键词
gamma-Aminobutyric acid; Ischemia/reperfusion; Acute kidney injury; Renal sympathetic nerve activity; Norepinephrine overflow
资金
- Ministry of Education, Culture, Sports, Science and Technology
Enhanced renal sympathetic nerve activity during ischemic period and the renal venous norepinephrine overflow after reperfusion play important roles in the development of ischemic acute kidney injury. We investigated the effect of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter mainly in the central nervous system, oil ischemia/reperfusion-induced acute kidney injury in anesthetized rats. Ischemic acute kidney injury was induced by clamping the left renal artery and vein for 45 min followed by reperfusion 2 weeks after the contralateral nephrectomy. Intravenous injection of GABA (10 and 50 mu mol/kg) to ischemic acute kidney injury rats dose-dependently Suppressed the enhanced renal sympathetic nerve activity during the renal ischemia, the renal venous norepinephrine overflow after reperfusion and attenuated the ischemia/reperfusioin-induced renal dysfunction with histological damage. Intravenous injection of CGP52432 (0.1 mu mol/kg), a selective GABA(B) receptor antagonist, eliminated the preventive effect by GABA (50 mu mol/kg) on ischemic acute kidney injury. In contrast, intravenous injection of baclofen (1 mu mol/kg), a selective GABA(B) receptor agonist, attenuated the ischemia/reperfusion-induced renal injury equivalent to GABA (50 mu mol/kg). These results indicate that GABA prevents the development of ischemia/reperfusion-induced acute kidney injury presumably via GABA(B) receptor, by suppressing the enhanced renal sympathetic nerve activity during ischemia and the increased norepinephrine overflow from renal sympathetic nerve ending. (C) 2009 Elsevier B.V. All rights reserved.
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