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首页> 外文期刊>Cardiovascular therapeutics >Valsartan improves endothelial dysfunction in hypertension: a randomized, double-blind study.
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Valsartan improves endothelial dysfunction in hypertension: a randomized, double-blind study.

机译：缬沙坦可改善高血压中的内皮功能障碍：一项随机，双盲研究。

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Endothelial dysfunction can predict cardiac outcomes in hypertension and reversing this abnormality has become an attractive therapeutic objective. We tested the hypothesis that blocking the angiotensin type 1 (AT(1)) receptor with valsartan in comparison with amlodipine would lead to an improvement in forearm resistance artery endothelial dysfunction. In total, 25 hypertensive subjects (mean age 60 years, SD 8) with a mean daytime ambulatory blood pressure (BP) of 154 (10)/97 (6) mmHg were randomized following a 3-week placebo run-in period to a double-blind, crossover trial of 16-week treatment periods with either valsartan or amlodipine, separated by a 3-week washout period. Intra-arterial infusions of acetylcholine (ACh) and N(G)-monomethyl-L-arginine (L-NMMA) were used to assess stimulated and basal endothelium-dependent nitric oxide (NO) release, respectively. Coinfusion of ACh and L-NMMA was employed to investigate the existence of an NO-independent vasodilatory pathway. Valsartan and amlodipine each lowered the clinical BP to the same extent (139 [7]/87 [6] and 139 [11]/89 [4] mmHg, respectively). The vasodilatory response to ACh was significantly increased with valsartan (maximal percentage change in forearm blood flow (max. DeltaFBF%) 301 [47] vs. 185 [34], mean [SEM]; P < 0.05) as compared with placebo, but remained unchanged with amlodipine. Both valsartan and amlodipine similarly increased the vasoconstrictive response to L-NMMA (max. DeltaFBF%-43 [5], -42 [5], respectively, vs. -26 [3] baseline; P < 0.001). The vasodilatory response after coinfusion of ACh and L-NMMA was significantly (P < 0.05) enhanced only with valsartan. Valsartan reserved peripheral endothelial dysfunction through both NO-dependent and -independent pathways, while for the same degree of BP control, amlodipine had only a partial effect on NO bioactivity.
机译：内皮功能障碍可以预测高血压的心脏预后，扭转这种异常已成为有吸引力的治疗目标。我们测试了以下假设：与氨氯地平相比，用缬沙坦阻断1型血管紧张素（AT（1））受体会导致前臂阻力动脉内皮功能障碍的改善。在总共3周的安慰剂磨合期后，将25名平均日间动态血压（BP）为154（10）/ 97（6）mmHg的高血压受试者（平均年龄60岁，SD 8）随机分为两组。缬沙坦或氨氯地平治疗16周的双盲，交叉试验，间隔3周的洗脱期。动脉内注入乙酰胆碱（ACh）和N（G）-单甲基-L-精氨酸（L-NMMA）分别评估刺激和基础内皮依赖性一氧化氮（NO）的释放。 ACh和L-NMMA的共输注用于研究不依赖NO的血管舒张途径的存在。缬沙坦和氨氯地平均将临床血压降低至相同程度（分别为139 [7] / 87 [6]和139 [11] / 89 [4] mmHg）。与安慰剂相比，缬沙坦显着提高了对ACh的血管舒张反应（前臂血流最大百分比变化（最大DeltaFBF％）301 [47]与185 [34]，平均值[SEM]; P <0.05），但是氨氯地平维持不变。缬沙坦和氨氯地平都类似地增加了对L-NMMA的血管收缩反应（分别为最大DeltaFBF％-43 [5]，-42 [5]和-26 [3]基线; P <0.001）。仅使用缬沙坦时，ACh和L-NMMA共融合后的血管舒张反应显着增强（P <0.05）。缬沙坦通过NO依赖性和非依赖性途径保留了外周血管内皮功能障碍，而对于相同程度的BP控制，氨氯地平对NO的生物活性仅具有部分作用。

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