Aggarwal Nitin T, Pfister Sandra L, Gauthier Kathryn M, Chawengsub Yuttana, Baker John E, Campbell William B
Dept. of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226, USA.
Am J Physiol Heart Circ Physiol. 2009 Mar;296(3):H678-88. doi: 10.1152/ajpheart.00777.2008. Epub 2008 Dec 26.
15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETAs) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial relaxations to agonists. We tested the effect of hypoxia on 15-LO-1 expression, THETA and HEETA synthesis, and relaxations in rabbit arteries. The incubation of rabbit aortic endothelial cells and isolated aortas in 0.7% O(2) increased 15-LO-1 expression. Rabbits were housed in a hypoxic atmosphere of 12% O(2) for 5 days. 15-LO-1 expression increased in the endothelium of the arteries of rabbits in 12% O(2) compared with room air. THETA and HEETA synthesis was also enhanced in aortas and mesenteric arteries. AA hyperpolarized the smooth muscle cells in indomethacin- and phenylephrine-treated mesenteric arteries of hypoxic rabbits from -29.4 +/- 1 to -50.1 +/- 3 mV. The hyperpolarization to AA was less in arteries of normoxic rabbits (from -26.0 +/- 2 to -37 +/- 2 mV). This AA-induced hyperpolarization was inhibited by the 15-LO inhibitor BW-755C. Nitric oxide and prostaglandin-independent maximum relaxations to acetylcholine (79.7 +/- 2%) and AA (38.3 +/- 4%) were enhanced in mesenteric arteries from hypoxic rabbits compared with the normoxic rabbits (49.7 +/- 6% and 19.9 +/- 2%, respectively). These relaxations were inhibited by BW-755C and nordihydroguaiaretic acid. Therefore, hypoxia increased the relaxations to agonists in the rabbit mesenteric arteries by enhancing endothelial 15-LO-1 expression and synthesis of the hyperpolarizing factors THETA and HEETA.
15-脂氧合酶(15-LO-1)将花生四烯酸(AA)代谢为11,12,15-三羟基二十碳三烯酸(THETAs)和15-羟基-11,12-环氧二十碳三烯酸(HEETA),这些物质可使兔动脉扩张。内皮细胞15-LO-1表达增加可增强动脉对激动剂的舒张反应。我们测试了缺氧对兔动脉中15-LO-1表达、THETA和HEETA合成以及舒张反应的影响。将兔主动脉内皮细胞和离体主动脉置于0.7% O₂中孵育可增加15-LO-1表达。将兔子置于含12% O₂的低氧环境中5天。与在空气中饲养的兔子相比,处于12% O₂环境中的兔子动脉内皮中15-LO-1表达增加。主动脉和肠系膜动脉中THETA和HEETA的合成也增强。在低氧兔子经吲哚美辛和去氧肾上腺素处理的肠系膜动脉中,AA使平滑肌细胞超极化,从-29.4±1 mV变为-50.1±3 mV。在常氧兔子的动脉中,AA引起的超极化程度较小(从-26.0±2 mV变为-37±2 mV)。这种AA诱导的超极化被15-LO抑制剂BW-755C抑制。与常氧兔子相比,低氧兔子肠系膜动脉中对乙酰胆碱(79.7±2%)和AA(38.3±4%)的一氧化氮和前列腺素非依赖性最大舒张反应增强(常氧兔子分别为49.7±6%和19.9±2%)。这些舒张反应被BW-755C和去甲二氢愈创木酸抑制。因此,缺氧通过增强内皮细胞15-LO-1表达以及超极化因子THETA和HEETA的合成,增加了兔肠系膜动脉对激动剂的舒张反应。