Rabkin S W
Department of Medicine, University Hospital (Shaughnessy), University of British Columbia, Vancouver, Canada.
J Clin Pharmacol. 1993 Mar;33(3):286-91. doi: 10.1002/j.1552-4604.1993.tb03958.x.
The objective of this article is to focus on the antihypertensive agents blocking adrenergic receptors, both alpha and beta blockers, and attempt to construct potential explanations for their effects on lipids in a mechanistic manner. The essential thesis is that adrenergic control of lipid metabolism is responsible for the effect on lipids and lipoproteins of antihypertensive agents that block adrenergic receptors. Agonists and antagonists show the opposite action on lipoprotein lipase, lecithin:cholesterol acyltransferase (LCAT) and LDL-cholesterol uptake by LDL receptors in a manner that might explain the findings of increases in triglycerides and LDL cholesterol with decreases in HDL cholesterol in patients receiving beta blockers without intrinsic sympathomimetic activity and the reverse in patients on treatment with alpha adrenergic receptor blockers.
本文的目的是聚焦于阻断肾上腺素能受体的抗高血压药物,即α和β受体阻滞剂,并试图以机制性的方式构建对其脂质效应的潜在解释。基本论点是,脂质代谢的肾上腺素能控制是阻断肾上腺素能受体的抗高血压药物对脂质和脂蛋白产生影响的原因。激动剂和拮抗剂对脂蛋白脂肪酶、卵磷脂胆固醇酰基转移酶(LCAT)以及低密度脂蛋白受体摄取低密度脂蛋白胆固醇具有相反的作用,这种方式可能解释了在接受无内在拟交感活性的β受体阻滞剂治疗的患者中甘油三酯和低密度脂蛋白胆固醇升高而高密度脂蛋白胆固醇降低,以及接受α肾上腺素能受体阻滞剂治疗的患者中情况相反的研究结果。