AHA Comprehensive Hypertension Center, Department of Medicine, Section of Endocrinology, Diabetes, and Metabolism, The University of Chicago Medicine, 5841 S. Maryland Ave. MC 1027, Chicago, IL, 60637, USA.
Curr Hypertens Rep. 2019 Feb 12;21(2):12. doi: 10.1007/s11906-019-0920-4.
This is an update of data regarding changes in blood pressure using sodium-glucose co-transporter 2 inhibitors (SGLT2i) for the treatment of diabetes. The mechanism of blood pressure lowering by SGLT2i was thought to be due to their osmotic diuretic effects. New data, however, has emerged from meta-analyses and studies of people with impaired kidney function demonstrating similar or greater magnitudes of blood pressure reduction in the absence of significant glycosuria. Potential additional mechanisms are proposed and reviewed.
Two separate meta-analyses in over 10,000 participants combined demonstrate an average of 4/2 mmHg reduction in blood pressure by SGLT2i. This includes consistency between measurements of in-office and ambulatory blood pressure monitoring. This reduction extends to decreases in nocturnal blood pressure of 2.6 mmHg systolic pressure. These reductions in blood pressure by SGLT2i are also present when added to ongoing treatment with ACE inhibitors or ARBs. In one study, dapagliflozin, when added to a regimen of a renin-angiotensin-aldosterone system (RAAS) antagonist and a diuretic, further lowered in-office systolic pressure by 2.4 mmHg. In contrast, when prescribed to those on a RAAS antagonist plus a calcium channel blocker or RAAS antagonist plus a beta blocker, systolic pressure decreased 5.4 mmHg. Lastly, post hoc analyses of major cardiovascular outcome trials across the spectrum of estimated glomerular filtration rates from 30 to 80 ml/min/1.73 m2 demonstrated similar magnitudes of BP reduction in spite of far less reduction in glucosuria among those with advanced kidney disease. Moreover, recent data implicate the potential for increased ketones associated with SGLT2i contributing to blood pressure lowering in advanced-stage kidney disease. SGLT2i are well established to lower blood pressure. Their mechanism appears to be multifactorial and has a hemodynamic as well as metabolic component contributing to this reduction.
这是一篇关于使用钠-葡萄糖协同转运蛋白 2 抑制剂（SGLT2i）治疗糖尿病时血压变化数据的更新。SGLT2i 降低血压的机制被认为是由于其渗透利尿作用。然而，来自荟萃分析和肾功能受损人群的研究的数据表明，在没有明显糖尿的情况下，SGLT2i 同样或更大程度地降低血压。提出并回顾了潜在的其他机制。
两项分别对超过 10000 名参与者进行的荟萃分析表明，SGLT2i 平均可降低 4/2mmHg 的血压。这包括在诊室和动态血压监测中测量的一致性。这一降低还包括夜间收缩压降低 2.6mmHg。当 SGLT2i 加入正在进行的 ACE 抑制剂或 ARB 治疗时，血压也会降低。在一项研究中，达格列净在与肾素-血管紧张素-醛固酮系统（RAAS）拮抗剂和利尿剂联合使用时，诊室收缩压进一步降低了 2.4mmHg。相比之下，当处方给 RAAS 拮抗剂加钙通道阻滞剂或 RAAS 拮抗剂加β受体阻滞剂的患者时，收缩压下降了 5.4mmHg。最后，对估计肾小球滤过率从 30 到 80ml/min/1.73m2 的主要心血管结局试验的事后分析表明，尽管在晚期肾病患者中，糖尿减少幅度较小，但血压降低幅度相似。此外，最近的数据表明，SGLT2i 可能与酮体增加有关，这有助于晚期肾脏疾病的血压降低。SGLT2i 已被证实可降低血压。其机制似乎是多因素的，具有血流动力学和代谢成分，有助于降低血压。
