Duarte Julio D, Cooper-DeHoff Rhonda M
Department of Pharmacotherapy and Translational Research, College of Pharmacy, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610-0486, USA.
Expert Rev Cardiovasc Ther. 2010 Jun;8(6):793-802. doi: 10.1586/erc.10.27.
Thiazide and thiazide-like diuretics are among the most commonly used antihypertensives and have been available for over 50 years. However, the mechanism by which these drugs chronically lower blood pressure is poorly understood. Possible mechanisms include direct endothelial- or vascular smooth muscle-mediated vasodilation and indirect compensation to acute decreases in cardiac output. In addition, thiazides are associated with adverse metabolic effects, particularly hyperglycemia, and the mechanistic underpinnings of these effects are also poorly understood. Thiazide-induced hypokalemia, as well as other theories to explain these metabolic disturbances, including increased visceral adiposity, hyperuricemia, decreased glucose metabolism and pancreatic beta-cell hyperpolarization, may play a role. Understanding genetic variants with differential responses to thiazides could reveal new mechanistic candidates for future research to provide a more complete understanding of the blood pressure and metabolic response to thiazide diuretics.
噻嗪类和噻嗪样利尿剂是最常用的抗高血压药物之一,已应用超过50年。然而,这些药物长期降低血压的机制尚不清楚。可能的机制包括直接的内皮或血管平滑肌介导的血管舒张以及对心输出量急性减少的间接代偿。此外,噻嗪类药物会引起不良代谢效应,尤其是高血糖,而这些效应的机制基础也不清楚。噻嗪类药物引起的低钾血症以及其他解释这些代谢紊乱的理论,包括内脏肥胖增加、高尿酸血症、葡萄糖代谢降低和胰腺β细胞超极化,可能都起了作用。了解对噻嗪类药物有不同反应的基因变异,可能会揭示新的机制候选物,以供未来研究,从而更全面地了解噻嗪类利尿剂对血压和代谢的反应。