Huang Y T, Chang S P, Lin H C, Yang M C, Hong C Y
Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
J Hepatol. 1997 Feb;26(2):376-81. doi: 10.1016/s0168-8278(97)80055-4.
BACKGROUND/AIMS: Venous hyporesponsiveness in portal hypertension has been reported previously by us. The present study was undertaken to investigate possible changes of phosphoinositide signal transduction pathway in the portal veins from portal hypertensive rats
Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for measurement of [3H]inositol phosphate responses to both receptor- and nonreceptor-mediated stimuli.
Basal [3H]inositol phosphate formation was similar between the two groups. Both phenylephrine and angiotensin II stimulated [3H]inositol phosphate formation in portal veins, but the responses were attenuated in the portal hypertensive group. In contrast, the [3H]inositol phosphate formation by nonreceptor-mediated stimuli (GTP gamma S, NaF/AlCl3, and phospholipase C) was similar between the two groups.
Our results showed that the receptor-mediated [3H]inositol phosphate formation was attenuated, while the non-receptor-mediated formation was unaltered, in the portal vein from portal hypertensive rats.
背景/目的：我们之前报道过门静脉高压症中存在静脉低反应性。本研究旨在探讨门静脉高压大鼠门静脉中磷酸肌醇信号转导途径可能发生的变化。
通过部分门静脉结扎诱导门静脉高压。术后14天，取出门静脉以测量对受体介导和非受体介导刺激的[3H]肌醇磷酸反应。
两组之间基础[3H]肌醇磷酸生成相似。去氧肾上腺素和血管紧张素II均刺激门静脉中[3H]肌醇磷酸生成，但门静脉高压组的反应减弱。相反，非受体介导刺激（GTPγS、NaF/AlCl3和磷脂酶C）引起的[3H]肌醇磷酸生成在两组之间相似。
我们的结果表明，门静脉高压大鼠门静脉中受体介导的[3H]肌醇磷酸生成减弱，而非受体介导的生成未改变。
