Tanaka Masami, Sekioka Risa, Nishimura Takeshi, Ichihara Atsuhiro, Itoh Hiroshi
Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Diabetes Res Clin Pract. 2014 Dec;106(3):504-10. doi: 10.1016/j.diabres.2014.09.056. Epub 2014 Oct 25.
Hypertension stimulates the sympathetic nervous system and this phenomenon is exacerbated by diabetes mellitus. We investigated the effects of cilnidipine, an N/L-type calcium channel blocker, on aspects of this system in patients with type 2 diabetes mellitus.
In 33 hypertensive patients with type 2 diabetes mellitus treated with a calcium channel blocker other than cilnidipine, we evaluated the influence of switching to cilnidipine on blood pressure, heart rate, catecholamine, plasma renin and aldosterone concentration, brain natriuretic peptide, urine liver-type fatty acid binding protein, and urinary albumin excretion ratio in the same patients by a cross-over design. Other biochemical parameters were also evaluated.
Switching to cilnidipine did not change blood pressure but caused reduction in catecholamine concentrations in blood and urine and plasma aldosterone concentration, accompanied by significant reduction in brain natriuretic peptide, urine liver-type fatty acid binding protein, and albumin excretion ratio. These parameters other than brain natriuretic peptide were significantly increased after cilnidipine was changed to the original calcium channel blocker.
In 33 hypertensive patients with type 2 diabetes mellitus, compared to other calcium channel blockers, cilnidipine suppressed sympathetic nerve activity and aldosterone, and significantly improved markers of cardiorenal disorders. Therefore, cilnidipine may be an important calcium channel blocker for use in combination with renin-angiotensin-aldosterone system inhibitors when dealing with hypertension complicated with diabetes mellitus.
高血压会刺激交感神经系统，而糖尿病会加剧这种现象。我们研究了N/L型钙通道阻滞剂西尼地平对2型糖尿病患者该系统各方面的影响。
在33例接受除西尼地平以外的钙通道阻滞剂治疗的2型糖尿病高血压患者中，我们采用交叉设计评估了换用西尼地平对同一患者的血压、心率、儿茶酚胺、血浆肾素和醛固酮浓度、脑钠肽、尿肝型脂肪酸结合蛋白以及尿白蛋白排泄率的影响。还评估了其他生化参数。
换用西尼地平后血压未改变，但导致血液和尿液中的儿茶酚胺浓度以及血浆醛固酮浓度降低，同时脑钠肽、尿肝型脂肪酸结合蛋白和白蛋白排泄率显著降低。将西尼地平换回原来的钙通道阻滞剂后，除脑钠肽外的这些参数显著升高。
在33例2型糖尿病高血压患者中，与其他钙通道阻滞剂相比，西尼地平抑制了交感神经活动和醛固酮，并显著改善了心肾疾病标志物。因此，在治疗合并糖尿病的高血压时，西尼地平可能是与肾素-血管紧张素-醛固酮系统抑制剂联合使用的重要钙通道阻滞剂。
