Bönner G, Toussaint C, Claus M, Fritschka E, Philipp T, Vetter H, Feltkamp H
Department of Internal Medicine II, University of Cologne, Merheim Hospital, Köln, F.R.G.
Agents Actions Suppl. 1992;38 ( Pt 3):294-303.
Primary hypertension is associated with a lack in renal kallikrein activity which might be one of the reasons for the blood pressure elevation. Some smaller and partially uncontrolled studies suggested that an oral substitution of glandular kallikrein lowers blood pressure by a kinin-mediated vasodilation and increased natriuresis. To test this hypothesis we treated in two studies over 100 patients with untreated mild to moderate primary hypertension (WHO I-II) for 5 resp. 12 weeks in a double blind randomized and placebo controlled manner with 1800 U glandular kallikrein orally. Blood pressure measurements were performed according to the two study designs after 3 and 5 resp. 8 and 12 weeks of treatment sphymomanometrically in the day time course. No significant changes in blood pressure by kallikrein treatment could be observed at any time. Neither renal kallikrein excretion, renin and ACE-activity nor blood glucose concentration in diabetics or non-diabetics was changed. Thus, we could undoubtedly demonstrate that oral applied glandular kallikrein has no effect on primary hypertension.
原发性高血压与肾激肽释放酶活性缺乏有关,这可能是血压升高的原因之一。一些规模较小且部分未得到充分控制的研究表明,口服腺体激肽释放酶可通过激肽介导的血管舒张和利钠作用增强来降低血压。为验证这一假设,我们在两项研究中以双盲随机和安慰剂对照的方式,用1800 U腺体激肽释放酶对100多名未经治疗的轻至中度原发性高血压(世界卫生组织I-II级)患者进行了治疗,治疗时间分别为5周和12周。在治疗3周和5周以及8周和12周后,根据两种研究设计在白天通过血压计进行血压测量。在任何时间均未观察到激肽释放酶治疗使血压发生显著变化。糖尿病患者和非糖尿病患者的肾激肽释放酶排泄、肾素和ACE活性以及血糖浓度均未改变。因此,我们可以明确证明口服腺体激肽释放酶对原发性高血压没有影响。