Involvement of nitric oxide and prostanoid on the endothelium -dependent vasodilatation by acetylcholine in the isolated rabbit renal artery |
Joo-heon Kim1, Cheol-soo Shim1, Seok-cheol Jeon2 |
1College of Veterinary Medicine and Institute of Animal Medicine, Gyeongsang National University 2Cardiac center, Masan Samsung General Hospital |
토끼 적출 신동맥에 있어서 acetylcholine에 의한 내피세포 의존성 이완작용에 대한 nitric oxide와 prostanoid의 연관성 |
김주헌1, 심철수1, 전석철2 |
1경상대학교 수의과대학, 동물의학연구소 2마산삼성병원 심장센터 |
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Abstract |
The effect of the nitric oxide synthase(NOS) inhibitor, $N^{G}$-nitro-L-arginine methyl ester (L-NAME), and the prostanoid synthesis inhibitor, indomethacin, on the vasodilatation produced in response to acetylcholine(Ach) on the isolated rabbit renal artery was examined. The vasodilatory reponses to Ach($10^{-8}-3{ imes}10^{-5}M$) were completely absent in thevessel which the endothelium had previous been removed. L-NAME($10^{-4}M$) significantly reduced the vasodilatory reponse to the Ach($10^{-8}-3{ imes}10^{-5}M$). When L-arginine ($10^{-3}M$) was also present in the organ bath along with L-NAME($10^{-4}M$), this inhibitory effect of L-NAME ($10^{-4}M$) on the vasodilatory response to Ach ($10^{-8}-3{ imes}10^{-5}M$) was significantly attenuated, Indomethacin ($10^{-6}M$) did not significantly affect the vasodilatory responses to Ach ($10^{-8}-3{ imes}10^{-5}M$). The inhibition by L-NAME ($10^{-4}M$) and indomethacin ($10^{-6}M$) on vasodilatory response to Ach was significantly greater than the inhibition due to L-NAME ($10^{-4}M$) alone. The present study has established that Ach induce relaxation via and endothelium-dependent mechanism, this relaxation to Ach involves both nitric oxide(NO) and prostanoid in the isolated rabbit renal artery. |
Key Words:
endothelium-dependent relaxation, nitric oxide, acetylcholine, indomethacin, renal artery, rabbit |
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