Holm M, Powell T, Casselbrant A, Johansson B, Fändriks L
Department of Physiology, Göteborg University, Sweden.
Dig Dis Sci. 2001 Aug;46(8):1765-71. doi: 10.1023/a:1010674109111.
It has previously been shown that mucosal nitric oxide synthase (NOS) is involved in acid-induced duodenal mucosal alkaline secretion. The primary aim of the present study was to elucidate which isoform of NOS is responsible in rats. Immunohistochemistry showed that inducible NOS (iNOS) was constitutively expressed in villous epithelial cells. Exposing the duodenal mucosa to 10 mM HCl resulted in an increased duodenal mucosal alkaline secretion. This response was totally inhibited by intraluminal administration of a selective inhibitor of iNOS (L-N6-1-iminoethyl-lysine). One hour after the acid exposure, western blot technique showed a marked increase in mucosal iNOS expression. A second acid exposure resulted in a further stimulation of alkaline secretion. These data suggest that exposure of the duodenal mucosa to HCI initiates an increased mucosal alkaline secretion, via NO synthesis mediated by iNOS located in the epithelial cells of the villi. In addition, luminal acid stimulates expression of iNOS.
先前的研究表明，黏膜一氧化氮合酶（NOS）参与酸诱导的十二指肠黏膜碱性分泌。本研究的主要目的是阐明大鼠中哪种NOS同工型起作用。免疫组织化学显示，诱导型NOS（iNOS）在绒毛上皮细胞中组成性表达。将十二指肠黏膜暴露于10 mM盐酸会导致十二指肠黏膜碱性分泌增加。腔内给予iNOS的选择性抑制剂（L-N6-1-亚氨基乙基赖氨酸）可完全抑制这种反应。酸暴露1小时后，蛋白质印迹技术显示黏膜iNOS表达显著增加。再次酸暴露导致碱性分泌进一步增加。这些数据表明，十二指肠黏膜暴露于盐酸会通过位于绒毛上皮细胞中的iNOS介导的NO合成引发黏膜碱性分泌增加。此外，腔内酸刺激iNOS的表达。
