REGULATION OF ATP-SENSITIVE K+ CHANNELS BY CHRONIC GLYBURIDE AND PINACIDIL ADMINISTRATION

被引:13
作者
GOPALAKRISHNAN, M [1 ]
TRIGGLE, DJ [1 ]
机构
[1] SUNY BUFFALO,SCH PHARM,DEPT BIOCHEM PHARMACOL,126 COOKE HALL,BUFFALO,NY 14260
关键词
D O I
10.1016/0006-2952(92)90080-3
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Treatment of rats with the K(ATP)+ channel antagonist sulfonylurea, glyburide (3 mg/kg/day, i.p., every 12 hr for 9 days). increased the B(max) value of [H-3]glyburide binding to heart and whole brain total membranes by 30 and 24 %, respectively. The ligand affinity was unaltered. Treatment with the K+ channel activator, pinacidil (20 mg/kg/day, i.p., every 12 hr tor 9 days), did not alter the B(max) value for cardiac [H-3]glyburide binding sites, but decreased the B(max) value in the brain by 21 %. Chronic administration of hydralazine, which caused an acute reduction in systolic blood pressure equivalent to that of pinacidil, did not alter [H-3]glyburide binding in either heart or brain. Treatment with glyburide, pinacidil or hydralazine did not alter L-type calcium channels, assessed by [H-3]PN 200 110 binding, in cardiac and brain membranes or small size Ca2+-activated K+ channels in brain assessed by [I-125]apamin binding. These studies show that the ATP-sensitive class of K+ channels can be regulated following chronic drug treatment in similar fashion to other receptor and channel systems.
引用
收藏
页码:1843 / 1847
页数:5
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