Mechanisms Underlying Relaxations Caused by Angiotensin II and Its Analogs in Isolated Rabbit Mesenteric Artery
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- 영문명
- Mechanisms Underlying Relaxations Caused by Angiotensin II and Its Analogs in Isolated Rabbit Mesenteric Artery
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Ki Whan Hong Ji Young Park Chi Dae Kim Won Suk Lee Byung Yong Rhim,
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제1권 제4호, 393~402쪽, 전체 10쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 1997.01.01
구매일시로부터 72시간 이내에 다운로드 가능합니다.
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국문 초록
영문 초록
In the present study, we characterized the angiotensin II (AII)-induced relaxations in the phenylephrine- precontracted rabbit mesenteric arteries with endothelium. 1) AII-induced relaxation was consistently observed in the rabbit mesenteric arteries with and without endothelium, but not in the aortic segment with endothelium. 2) AII-induced endothelium-dependent relaxation was markedly inhibited by Nw-nitro- L-arginine (L-NNA, 100 ㄍM), methylene blue (10 ㄍM) and LY83583 (10 ㄍM), respectively. 3) Inhibition of cyclooxygenase with indomethacin (10 ㄍM) strongly decreased the vasorelaxant response to AII irrespective of the presence of endothelium. 4) 7-Ethoxyresorufin (1 ㄍM) and clotrimazole (1 ㄍM), inhibitors of cytochrome P-450-dependent arachidonic acid metabolism, greatly attenuated the vasodilator response to AII. 5) Carbacyclin, arachidonic acid and prostaglandin F2α (PGF2α) caused concentration-dependent relaxations in the mesenteric artery with endothelium, which were inhibited by L-NNA and methylene blue. 6) AII and PGF2α significantly stimulated cyclic GMP formation in the mesenteric arteries with endothelium, which was inhibited by L-NNA and methylene blue, respectively. 7) AII enhanced synthesis of PGF2α and 6-keto PGF1α from the arterial segments with endothelium, which was inhibitable by indomethacin, but not by L-NNA.
In conclusion, the vasorelaxant responses to AII of the rabbit mesenteric artery with endothelium are subserved by arachidonic acid and its metabolites produced via activation of cyclooxygenase and cytochrome P-450 enzyme as well as by nitric oxide.
목차
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