(R)-ACX, a pancreatic β-cell selective sulfonylurea, does not aggravate myocardial ischemia-reperfusion damage
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- 作者：Iyuki Namekata ; Yusuke Yamaguchi ; Shuhei Moriguchi ; Satoshi Yamazaki ; Akihiko Terasawa ; Reiko Yamagishi ; Tokiko Aikawa ; Tomoaki Saito ; Katsumi Kurashima ; Kenji Seri ; Yorishige Imamura ; Hiroyuki Akita
- 关键词：Heart ; Ischemia-reperfusion ; (R)-ACX
- 刊名：European Journal of Pharmacology
- 出版年：2007
- 出版时间：22 December 2007
- 年：2007
- 卷：577
- 期：1-3
- 页码：211-218
- 全文大小：303 K
文摘
The organ selectivity and the effect on myocardial ischemia-reperfusion injury of (R)-acetoxyhexamide ((R)-ACX), a novel sulfonylurea, were examined. (R)-ACX, as well as glibenclamide, concentration-dependently stimulated insulin release from INS-1 cell, a cell line derived from pancreatic β-cells. The potency of (R)-ACX was about 1/10 of that of glibenclamide. In isolated guinea pig ventricular myocardial tissue, glibenclamide concentration-dependently inhibited the action potential shortening by NIP-121, an ATP-sensitive potassium channel opener, but (R)-ACX showed only slight inhibition. In isolated rat aortic rings contracted with norepinephrine, glibenclamide concentration-dependently inhibited the relaxation by NIP-121, while (R)-ACX showed only slight inhibition. In coronary-perfused guinea pig ventricular preparations, glibenclamide reduced the recovery of contractile force after ischemia-reperfusion, while (R)-ACX did not. In conclusion, (R)-ACX is a β-cell selective sulfonylurea which, unlike glibenclamide, does not aggravate cardiac ischemia-reperfusion damage.