Tomiyama H, Kimura Y, Mitsuhashi H, Kinouchi T, Yoshida H, Kushiro T, Doba N
The Third Department of Internal Medicine, Teikyo University School of Medicine, Ichihara Hospital, Chiba, Japan.
Hypertension. 1998 Jan;31(1 Pt 2):321-7. doi: 10.1161/01.hyp.31.1.321.
Abnormalities in fibrinolysis, endothelial function, and glucose and lipid metabolism have been reported in hypertension. This study was conducted to examine the interrelationships between fibrinolytic factors, glucose and lipid metabolism, and endothelial function in hypertension. The effects of administering an angiotensin converting enzyme inhibitor, benazepril, were also examined. Blood levels of the following substances were measured in patients with borderline and mild hypertension (n=50, 51+/-19 years) and in age-matched controls (n=10): total cholesterol, triglycerides, tissue plasminogen activator activity and antigen, and plasminogen activator inhibitor type 1 activity and antigen. Insulin sensitivity was assessed by oral glucose tolerance test, and endothelial function was assessed by evaluating changes in diameter of the brachial artery during reactive hyperemia as observed by ultrasonography. Activities of tissue plasminogen activator and plasminogen activator inhibitor type 1 were both elevated in the hypertensive patients. Stepwise multiple regression analysis showed that plasminogen activator inhibitor type 1 antigen correlated with insulin sensitivity, total cholesterol levels, and triglycerides levels (P<.01). Endothelial function was negatively correlated with tissue plasminogen activator activity and antigen (P<.01). The chronic administration of benazepril (5-10 mg/d) for 20 weeks improved insulin sensitivity, endothelial function (6.6+/-3.4-->9.0+/-2.5%, P<.01), and tissue plasminogen activator activity and antigen. These results indicate that abnormalities in fibrinolysis are associated with endothelial dysfunction as well as disorders of glucose and lipid metabolism in patients with borderline and mild hypertension. The treatment of such patients with benazepril appeared to improve the impairment in fibrinolysis and endothelial dysfunction.
高血压患者中已报道存在纤维蛋白溶解、内皮功能以及糖脂代谢异常。本研究旨在探讨高血压患者纤维蛋白溶解因子、糖脂代谢与内皮功能之间的相互关系。同时也研究了给予血管紧张素转换酶抑制剂贝那普利的效果。对临界高血压和轻度高血压患者(n = 50,年龄51±19岁)以及年龄匹配的对照组(n = 10)测定了以下物质的血药浓度:总胆固醇、甘油三酯、组织纤溶酶原激活物活性及抗原、纤溶酶原激活物抑制剂1型活性及抗原。通过口服葡萄糖耐量试验评估胰岛素敏感性,通过超声检查评估反应性充血期间肱动脉直径变化来评估内皮功能。高血压患者的组织纤溶酶原激活物和纤溶酶原激活物抑制剂1型的活性均升高。逐步多元回归分析显示,纤溶酶原激活物抑制剂1型抗原与胰岛素敏感性、总胆固醇水平和甘油三酯水平相关(P <.01)。内皮功能与组织纤溶酶原激活物活性及抗原呈负相关(P <.01)。连续20周给予贝那普利(5 - 10 mg/d)可改善胰岛素敏感性、内皮功能(6.6±3.4%→9.0±2.5%,P <.01)以及组织纤溶酶原激活物活性及抗原。这些结果表明,临界高血压和轻度高血压患者的纤维蛋白溶解异常与内皮功能障碍以及糖脂代谢紊乱有关。用贝那普利治疗此类患者似乎可改善纤维蛋白溶解和内皮功能障碍。