Bell F P
J Cardiovasc Pharmacol. 1985 May-Jun;7(3):443-8. doi: 10.1097/00005344-198505000-00005.
The effects of five antihypertensive agents on lipid biosynthesis from [1-14C]oleate were studied in rat liver minces. At a level of 1 mM, propranolol and prazosin increased the incorporation of [14C]oleate into diglycerides and cholesteryl esters by two- to fourfold and increased total phospholipid labeling by 20-30%. Chlorthalidone and metoprolol at 1 mM also stimulated the incorporation of [14C]oleate into phospholipids and diglycerides (20-50%) but did not affect its incorporation into triglycerides or cholesteryl esters. All four of the compounds statistically significantly inhibited the incorporation of [14C]oleate into phosphatidylcholine by 12-37% but stimulated incorporation into phosphatidylinositol by 17-95%. Nadolol differed from the other compounds in that it did not show selective effects but rather inhibited the incorporation of [14C]oleate into all lipid classes by approximately 50%. The data are discussed in terms of possible mechanisms involved in the lipid synthesis patterns and suggest the possibility that plasma lipid/lipoprotein changes observed in patients undergoing antihypertensive therapy may reflect, in part, altered hepatic lipid synthesis.
在大鼠肝匀浆中研究了五种抗高血压药物对[1-14C]油酸酯脂质生物合成的影响。在1 mM的浓度下，普萘洛尔和哌唑嗪使[14C]油酸酯掺入甘油二酯和胆固醇酯的量增加了两到四倍，并使总磷脂标记增加了20-30%。1 mM的氯噻酮和美托洛尔也刺激了[14C]油酸酯掺入磷脂和甘油二酯（20-50%），但不影响其掺入甘油三酯或胆固醇酯。所有这四种化合物在统计学上均显著抑制[14C]油酸酯掺入磷脂酰胆碱达（12-37%），但刺激其掺入磷脂酰肌醇达（17-95%）。纳多洛尔与其他化合物不同，它没有显示出选择性作用，而是使[14C]油酸酯掺入所有脂质类别中的量减少了约50%。从脂质合成模式中可能涉及的机制方面对数据进行了讨论，并提示接受抗高血压治疗的患者中观察到的血浆脂质/脂蛋白变化可能部分反映了肝脏脂质合成的改变。
