Mechanism of vasodilatation induced by substance P in isolated rabbit renal artery |
Joo-heon Kim1, Seok-cheol Jeon2, Yonggeun Hong3 |
1College of Veterinary Medicine and Institute of Animal Medicine, Gyeongsang National University 2Cardiac center Masan Samsung General Hospital 3Department of Internal Medicine-Cardiology, University of Texas Southwestern Medical Center at Dallas |
토끼 적출 신동맥에 있어서 substance P에 의한 이완작용 기전 |
김주헌1, 전석철2, 홍용근3 |
1경상대학교 수의과대학 동물의학연구소 2마산삼성병원 심장센터 3 |
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Abstract |
The effects of removing the endothelium on the vasodilatory response to substance P, calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) was examined in the isolated rabbit renal artery. The vasodilator response to substance P ($0.1{mu}M$) was completely absent in vessels in which the endothelium had previously been removed. There was no significant difference in the vasodilatation produced in response to CGRP ($0.1{mu}M$), or VIP ($0.1{mu}M$) in the intact and removed-endothelium rabbit renal artery segments. L-NAME ($100{mu}M$) significantly reduced the vasodilatory response to substance P ($0.1{mu}M$). This inhibition was significantly attenuated when L-arginine (10 mM) was also present in the organ bath along with L-NAME ($100{mu}M$). Indomethacin ($1{mu}M$) did not significantly affect the vasodilatation produced in response to substance P ($0.1{mu}M$). The inhibitory effect of L-NAME ($100{mu}M$) and indomethacin ($1{mu}M$) on the vasodilatory response to substance P ($0.1{mu}M$) was not significantly different from that produced by L-NAME ($100{mu}M$) alone. This study indicates that substance P induced vasodilatation via an endothelium-dependent mechanism in the isolated rabbit renal artery. It also established that CGRP and VIP induced vasodilatation by an endothelium-independent mechanism and substance P-induced vasodilatation is at least partially via NO. |
Key Words:
vasodilatation, nitric oxide, substance P, calcitonin gene-related peptide, vasoactive intestinal peptide, renal artery, rabbit |
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