Weidmann P, Gerber A, Mordasini R
Hypertension. 1983 Sep-Oct;5(5 Pt 2):III120-31. doi: 10.1161/01.hyp.5.5_pt_2.iii120.
Several drugs used for standard antihypertensive therapy may also interact with the lipoprotein metabolism. The following has been observed after 1 to 12 months of treatment. Various thiazide-type diuretics may significantly increase the potentially atherogenic serum low-density-lipoprotein cholesterol (LDL-C) and/or very-LDL-C-fractions, while the antiatherogenic high-density-lipoprotein cholesterol (HDL-C) is largely unchanged. Certain loop-diuretics also increase the LDL-C/HDL-C ratio and both types of diuretics elevated serum triglycerides (Tg) in some but not all studies. LDL-C was increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women, but not in chlorthalidone-treated premenopausal women. The latter may be protected from this effect. Only two diuretics evaluated, namely indapamide and spironolactone, had no apparent influence on lipoproteins. Beta-blocker monotherapy may often increase Tg and slightly decrease HDL-C. The magnitude of these changes did not distinctly differ between highly cardioselective and nonselective beta-blockers, but it was less pronounced on beta-blockers than on those without intrinsic sympatholytic activity. Other sympatholytics such as reserpine, methyldopa, clonidine, debrisoquine, the alpha-beta-blocker labetalol, or the postsynaptic alpha-blocker, prazosin, did not affect or even slightly decrease Tg or total C, LDL-C, and very-LDL-C values. With combinations, a tendency for increased Tg and lower HDL-C was also apparent during thiazide-type diuretic-beta-blocker therapy. However, diuretic-induced increases in LDL-C were prevented or reversed by concomitant beta-blockade, but not by reserpine, methyldopa, or clonidine. Monotherapy with the potent direct vasodilator, carprazidil, improved blood pressure and significantly increased HDL-C. Prospective long-term studies are needed to clarify the course and the pathogenic and prognostic relevance of lipoprotein changes induced by certain diuretics or beta-blockers.
几种用于标准抗高血压治疗的药物也可能与脂蛋白代谢相互作用。在治疗1至12个月后观察到以下情况。各种噻嗪类利尿剂可能会显著增加具有潜在致动脉粥样硬化作用的血清低密度脂蛋白胆固醇（LDL-C）和/或极低密度脂蛋白胆固醇（VLDL-C）组分，而具有抗动脉粥样硬化作用的高密度脂蛋白胆固醇（HDL-C）基本保持不变。某些袢利尿剂也会增加LDL-C/HDL-C比值，并且在一些（但并非所有）研究中，这两种类型的利尿剂都会使血清甘油三酯（Tg）升高。接受利尿剂治疗的男性和接受氯噻酮治疗的绝经后女性的LDL-C升高，但接受氯噻酮治疗的绝经前女性的LDL-C未升高。后者可能免受这种影响。仅评估的两种利尿剂，即吲达帕胺和螺内酯，对脂蛋白没有明显影响。β受体阻滞剂单药治疗通常可能会使Tg升高并使HDL-C略有降低。高度心脏选择性和非选择性β受体阻滞剂之间这些变化的幅度没有明显差异，但在β受体阻滞剂上比在没有内在交感神经溶解活性的药物上不太明显。其他交感神经阻滞剂，如利血平、甲基多巴、可乐定、地昔帕明、α-β受体阻滞剂拉贝洛尔或突触后α受体阻滞剂哌唑嗪，不会影响甚至会轻微降低Tg或总胆固醇、LDL-C和VLDL-C值。联合用药时，噻嗪类利尿剂-β受体阻滞剂治疗期间也明显有Tg升高和HDL-C降低的趋势。然而，利尿剂引起的LDL-C升高可通过同时使用β受体阻滞剂来预防或逆转，但不能通过利血平、甲基多巴或可乐定来预防或逆转。强效直接血管扩张剂卡普地尔单药治疗可改善血压并显著增加HDL-C。需要进行前瞻性长期研究以阐明某些利尿剂或β受体阻滞剂引起的脂蛋白变化的过程及其致病和预后相关性。
