Orito K, Satoh K, Taira N
Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan.
Jpn J Pharmacol. 1992 Nov;60(3):295-7. doi: 10.1254/jjp.60.295.
Vasodepressor mechanisms of adenosine were investigated in spinally-anesthetized dogs. An i.v.-infusion of adenosine (0.1-10 mumol/kg/min) caused a slowly developing and sustained decrease in blood pressure (BP). This vasodepression was antagonized by glibenclamide, a blocker of ATP-sensitive K+ (KATP) channels. On the other hand, a transient decrease in BP caused by a single bolus i.v.-injection of adenosine was not antagonized by glibenclamide in our previous study. These results suggested that the opening of KATP channels is gradually recruited in the vasodepressor mechanisms for adenosine-induced sustained vasodepression.
在脊髓麻醉的犬中研究了腺苷的血管减压机制。静脉输注腺苷(0.1 - 10 μmol/kg/分钟)导致血压(BP)缓慢发展并持续下降。这种血管舒张作用被格列本脲(一种ATP敏感性钾通道阻滞剂)所拮抗。另一方面,在我们之前的研究中,单次静脉推注腺苷引起的血压短暂下降并未被格列本脲所拮抗。这些结果表明,在腺苷诱导的持续性血管舒张的血管减压机制中,ATP敏感性钾通道的开放是逐渐被激活的。