Tang F D, Yonehara N, Imai Y, Takiuchi S, Inoki R, Bian R L
Department of Pharmacology, Faculty of Dentistry, Osaka University, Japan.
Zhongguo Yao Li Xue Bao. 1994 May;15(3):232-4.
Contribution of kallikrein-kinin system to heat-induced substance P (SP) release into the periphery was studied by using plasma kininogens-deficient strain Brown Norway Katholiek (B/N-Ka) and normal strain Brown Norway Kitasato (B/N-Ki) rats. Bradykinin (BK) and SP levels in the sc perfusates of the hind instep were measured by radioimmunoassay. In B/N-Ki rat, immersion of hind paw into hot water (47 degrees C) for 20 min led to an increase of BK (43 +/- s 34 fmol.min-1) and SP (11.1 +/- 9.7 fmol.min-1) in the perfusate, whereas those in B/N-Ka rat (BK 1.3 +/- 1.0 fmol.min-1 (P < 0.01), SP 5.5 +/- 3.5 fmol.min-1 (P < 0.05)) were remarkably less. Heat-induced extravasation (leakage of Evans blue) in B/N-Ka rat was also less than that in B/N-Ki rat (P < 0.05). Results suggest that kallikrein-kinin system is involved in the release of SP into the periphery, ie, BK released into the extravascular space by noxious heat stimulation intervenes in SP release.
通过使用缺乏血浆激肽原的品系布朗挪威Katholiek（B/N-Ka）大鼠和正常品系布朗挪威北里（B/N-Ki）大鼠，研究了激肽释放酶-激肽系统对热诱导的P物质（SP）释放到外周的作用。通过放射免疫测定法测量后足背皮下灌流液中的缓激肽（BK）和SP水平。在B/N-Ki大鼠中，将后爪浸入47℃热水中20分钟导致灌流液中BK（43±34 fmol·min-1）和SP（11.1±9.7 fmol·min-1）增加，而在B/N-Ka大鼠中（BK 1.3±1.0 fmol·min-1（P<0.01），SP 5.5±3.5 fmol·min-1（P<0.05））则明显较少。B/N-Ka大鼠中热诱导的血管外渗（伊文思蓝渗漏）也比B/N-Ki大鼠少（P<0.05）。结果表明，激肽释放酶-激肽系统参与了SP释放到外周，即有害热刺激释放到血管外空间的BK干预了SP释放。
