신성고혈압쥐에서 Pinacidil에 의한 혈관 이완반응에 있어 산소유리기의 역할

Abstract

Evidence has emerged that oxygen-derived free radicals may induce vascular relaxations via ATP-sensitive K+ (KATP) channels and the level of free radicals is increased in animal models of hypertension. The present study was conducted to determine whether relaxations to an KATP channel opner, pinacidil, are increased in the aorta from two-kidney, one clip (2KIC) hypertensive rats and whether free radial scavengers reduce these relaxations. 2KIC hypertension was induced by clipping the left renal artery and age-matched control rats received a sham treatment. Rings of aortae without endothelium were suspended for isometric force recording. Relaxations to pinacidil (10-8 to 10-5 M), which are abolished by glibenclamide (10-5 M), were augmented in the aorta from 2KIC rats, compared to those from control rats. In the aorta from 2KIC rats, catalase (1200U/mL), but neither superoxide dismutase (150 U/mL) nor deferoxamine (10-4 M), reduced relaxations to pinacidil, whereas in the aorta from control rats, the free radical scavengers did not affect these relaxations. These results suggest that in 2KIC hypertension, vasorelaxation to an KATP channel opner is augmented and that hydrogen peroxide in smooth muscle cells may partly contribute to these relaxations.

Key words: KATP channel, Hydrogen peroxide, Vasorelaxation, Renal hypertension.