Gao X P
Department of Medicine, University of Illinois at Chicago 60612, USA.
Am J Physiol. 1998 Jan;274(1):R237-42. doi: 10.1152/ajpregu.1998.274.1.R237.
The purpose of this study was to determine whether tannic acid elicits neurogenic plasma exudation from the oral mucosa in vivo and, if so, whether this response is transduced in part by the L-arginine-nitric oxide (NO) biosynthetic pathway. Using intravital microscopy, we found that suffusion of tannic acid elicits significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-dextran (molecular mass 70 kDa) from the in situ hamster cheek pouch (P < 0.05). These effects are significantly attenuated by two selective, but structurally distinct, nonpeptide neurokinin-1 (NK1) receptor antagonists, CP-96,345 and RP-67580, but not by CP-96,344, the 2R,3R enantiomer of CP-96,345. NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, but not D-NAME, significantly attenuates tannic acid-induced responses. L-Arginine, but not D-arginine, reverses the attenuating effects of L-NAME. We conclude that tannic acid elicits L-arginine-NO biosynthetic pathway-dependent neurogenic plasma exudation from the in situ hamster cheek pouch.
本研究的目的是确定单宁酸在体内是否会引发口腔黏膜的神经源性血浆渗出，如果是，这种反应是否部分通过L-精氨酸-一氧化氮（NO）生物合成途径传导。通过活体显微镜检查，我们发现单宁酸灌注会引起浓度依赖性的显著渗漏部位形成，并增加异硫氰酸荧光素-葡聚糖（分子量70 kDa）从原位仓鼠颊囊的清除率（P < 0.05）。两种选择性但结构不同的非肽神经激肽-1（NK1）受体拮抗剂CP-96,345和RP-67580可显著减弱这些效应，但CP-96,345的2R,3R对映体CP-96,344则无此作用。NO合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）可显著减弱单宁酸诱导的反应，而D-NAME则无此作用。L-精氨酸可逆转L-NAME的减弱作用，而D-精氨酸则不能。我们得出结论，单宁酸会引发原位仓鼠颊囊的L-精氨酸-NO生物合成途径依赖性神经源性血浆渗出。
