Huang Y T, Yu P C, Lee M F, Lin H C, Hong C Y, Yang M C
Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Can J Physiol Pharmacol. 1995 Mar;73(3):378-82. doi: 10.1139/y95-048.
The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 x 10(-8) - 3 x 10(-6) M) and vasopressin (3 x 10(-10) - 3 x 10(-8) M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10(-7) - 10(-5) M) and vasopressin (10(-10) - 10(-8) M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.
本研究的目的是调查门静脉高压大鼠的血管收缩和肌醇磷酸反应。通过对Sprague-Dawley大鼠进行部分门静脉结扎（PVL）诱导门静脉高压。假手术大鼠作为对照。在手术后14天测定压力、血管收缩反应和肌醇磷酸反应。PVL大鼠的门静脉压力显著升高，而全身动脉压和心率降低。两组大鼠尾动脉对去甲肾上腺素（1×10⁻⁸ - 3×10⁻⁶ M）和血管加压素（3×10⁻¹⁰ - 3×10⁻⁸ M）均呈现剂量依赖性收缩反应。在所有剂量下，PVL大鼠对去甲肾上腺素的收缩反应与对照组相比显著降低。在较高剂量下，PVL大鼠对血管加压素的收缩反应显著降低。在尾动脉掺入肌醇-[³H]后，两组之间³H标记的磷脂酰肌醇水平（cpm/mg）相似。去甲肾上腺素（10⁻⁷ - 10⁻⁵ M）和血管加压素（10⁻¹⁰ - 10⁻⁸ M）剂量依赖性地刺激PVL大鼠和假手术大鼠尾动脉中³H标记的肌醇磷酸生成。然而，PVL大鼠的反应显著较低。结果表明，门静脉高压时血管收缩反应的减弱反映在磷脂酰肌醇信使系统中。
