Celık Turgay, Balta Sevket, Karaman Murat, Ahmet Ay Seyıt, Demırkol Saıt, Ozturk Cengız, Dınc Mustafa, Unal Hılmı U, Yılmaz M Ilker, Kılıc Selım, Kurt Gulcan, Tas A, Iyısoy Atıla, Quartı-Trevano Fosca, Fıcı Francesco, Grassı Guıdo
Department of Cardiology, Gulhane Medical Academy , Ankara , Turkey.
Blood Press. 2015 Feb;24(1):55-60. doi: 10.3109/08037051.2014.972816. Epub 2014 Nov 12.
Vascular inflammation plays an important role in the pathophysiology of hypertension and high levels of endocan may reflect ongoing vascular inflammation in hypertensive patients. In the present hypothesis-generating study, we aimed at investigating the comparative effects of amlodipine and valsartan on endocan levels in newly diagnosed hypertensive patients. The study population consisted of 37 untreated hypertensive patients who were randomized to the two treatment arms. After baseline assessment, each patient was randomly allocated to either 10 mg daily of amlodipine (n = 18, 7 males) or 160 mg daily of valsartan (n = 19, 3 males) and treated for a 3-month period. Sphygmomanometric blood pressure (BP) and serum endocan were measured before and every 2 weeks during drug treatment. There was no statistically significant difference between the two treatment arms as far as baseline socio-demographic and clinical characteristics are concerned. After a 3-month treatment period, systolic and diastolic BP values significantly reduced by antihypertensive treatment (p < 0.001). Furthermore, endocan levels were significantly decreased in both treatment arms (p < 0.05). However, amlodipine caused a greater percent decrease in circulating endocan levels compared with valsartan at the end of the treatment period. Both drugs reduced high sensitivity C-reactive protein values. However, the statistical significant difference vs baseline was achieved only in the group treated with amlodipine. No correlation was found between endocan plasma levels and BP reduction. The results of this hypothesis-generating study suggest that amlodipine and valsartan decrease endocan levels in newly diagnosed hypertensive patients. The effects, which are more evident with amlodipine, may contribute to the anti-inflammatory effects exerted by the two drugs on the vascular target.
血管炎症在高血压的病理生理学中起重要作用，而内皮糖蛋白水平升高可能反映高血压患者持续存在的血管炎症。在这项产生假设的研究中，我们旨在调查氨氯地平和缬沙坦对新诊断高血压患者内皮糖蛋白水平的比较影响。研究人群包括37名未经治疗的高血压患者，他们被随机分为两个治疗组。在基线评估后，每位患者被随机分配至每日服用10毫克氨氯地平组（n = 18，7名男性）或每日服用160毫克缬沙坦组（n = 19，3名男性），并接受为期3个月的治疗。在药物治疗前及治疗期间每2周测量血压计测量的血压（BP）和血清内皮糖蛋白。就基线社会人口统计学和临床特征而言，两个治疗组之间没有统计学显著差异。经过3个月的治疗期，收缩压和舒张压值通过降压治疗显著降低（p < 0.001）。此外，两个治疗组的内皮糖蛋白水平均显著降低（p < 0.05）。然而，在治疗期结束时，与缬沙坦相比，氨氯地平使循环内皮糖蛋白水平的下降百分比更大。两种药物均降低了高敏C反应蛋白值。然而，仅在氨氯地平治疗组中与基线相比达到统计学显著差异。未发现内皮糖蛋白血浆水平与血压降低之间存在相关性。这项产生假设的研究结果表明，氨氯地平和缬沙坦可降低新诊断高血压患者的内皮糖蛋白水平。氨氯地平的效果更明显，可能有助于这两种药物对血管靶点发挥抗炎作用。
