The Korean Journal of Physiology

The Korean Physiological Society (대한생리학회)
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Endothelium-dependent Contraction of Aorta in One-kidney, One-clip Goldblatt Hypertensive Rat

  • Jeon, Byeong-Hwa (Department of Physiology, College of Medicine, Chungnam National University) ;
  • Lee, Kug-Hee (Department of Physiology, College of Medicine, Chungnam National University) ;
  • Kim, Hoe-Suk (Department of Physiology, College of Medicine, Chungnam National University) ;
  • Kim, Se-Hoon (Department of Physiology, College of Medicine, Chungnam National University) ;
  • Chang, Seok-Jong (Department of Physiology, College of Medicine, Chungnam National University)
  • Published : 1996.12.30
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Abstract

The mechanism of impaired endothelium-dependent relaxation in the aorta of one-kidney, one clip Goldblatt hypertensive (1K,1C-GBH) rats was investigated. 8 week-old Wistar-Kyoto (WKY) rats were made hypertensive by left renal artery stenosis with contralateral nephrectomy. Endothelium-dependent relaxation was significantly reduced in 1K,1C-GBH rats as compared with WKY rats. However, the relaxation by sodium nitroprusside in 1K,1C-GBH rats was not reduced as compared with WKY rats. The impairment of endothelium-dependent relaxation in 1K,1C-GBH rats was partially restored by the pretreatment of indomethacin or SQ29548. When the nitric oxide production was inhibited by L-nitroarginine methyl ester, acetylcholine (ACh) induced a endothelium-dependent contraction that was greater in 1K,1C-GBH rats than in WKY rats. Endothelium-dependent contraction by ACh was completely abolished by indomethacin or SQ29548. However, imidazole, tranylcypromine and superoxide dismutase did not affect the endothelium-dependent contraction in 1K,1C-GBH rats. These results suggest that impaired endothelium-dependent relaxation in the 1K,1C-GBH rats might be due to the simultaneous release of EDCF, and that prostaglandin B2 may be involved as a mediator of endothelium-dependent contraction.

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