The Role of Oxygen-Derived Free Radicals in Vascular Relaxations to Pinacidil in Renal Hypertensive Rats.
- Author:
Seok CHOI
1
;
Im Joon YOO
;
Hee Wook WHI
;
Jae Yeoul JUN
;
Hyun Il KIM
;
Hye Rang SHIN
;
Hyun Jung OH
;
Jong Hoon CHUNG
;
Cheol Ho YEUM
Author Information
1. Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea. chyum@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
K(ATP) channels;
Hydrogen peroxide;
Vasorelaxation;
Renal hypertension
- MeSH:
Animals;
Aorta;
Catalase;
Deferoxamine;
Endothelium;
Free Radical Scavengers;
Free Radicals;
Glyburide;
Hydrogen Peroxide;
Hypertension;
Hypertension, Renal;
Models, Animal;
Myocytes, Smooth Muscle;
Pinacidil;
Placebos;
Rats;
Relaxation;
Renal Artery;
Salicylamides;
Superoxide Dismutase;
Vasodilation
- From:Korean Journal of Nephrology
2010;29(6):695-701
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Evidence has emerged that oxygen-derived free radicals may induce vascular relaxations via ATP-sensitive K+ (K(ATP)) 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 K(ATP) channel opener, pinacidil, are increased in the aorta from two-kidney, one clip (2K1C) hypertensive rats and whether free radial scavengers reduce these relaxations. METHODS: 2K1C 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. RESULTS: Relaxations to pinacidil (10(-8) to 10(-5) M), which are abolished by glibenclamide (10(-5) M), were augmented in the aorta from 2K1C rats, compared to those from control rats. In the aorta from 2K1C rats, catalase (1,200 U/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. CONCLUSION: These results suggest that in 2K1C hypertension, vasorelaxation to an KATP channel opener is augmented and that hydrogen peroxide in smooth muscle cells may partly contribute to these relaxations.