Weidmann P, Beretta-Piccoli C, Ziegler W, Hirsch D, de Châtel R D, Reubi F C
Klin Wochenschr. 1976 Aug 15;54(16):765-73. doi: 10.1007/BF01614293.
Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.
对55例原发性良性高血压患者的研究表明,β受体阻滞剂丁呋洛尔(22例患者)和普萘洛尔(33例患者)按1:4的剂量比使用时,尽管在内在拟交感活性方面特性不同,但具有相当的降压效果。β受体阻滞剂单药治疗使四分之一的患者血压恢复正常(低于140/90 mmHg)。在持续四至六周的β受体阻滞剂治疗期间,体重、血浆和血容量保持不变,平均血浆钾略有升高。普萘洛尔对血浆肾素活性(PRA)的抑制作用(-69%)比丁呋洛尔(-47%)更明显。两种β受体阻滞剂引起的血压下降均与治疗前PRA呈负相关(p<0.05)。普萘洛尔引起的血压变化也与PRA的相关变化相关(p<0.005);相比之下,丁呋洛尔未观察到这种关系。然而,丁呋洛尔的血压效应与尿去甲肾上腺素排泄的变化显著相关(r = 0.41;p<0.05)。平均而言,治疗前PRA低、正常或高的患者亚组显示出类似的治疗前去甲肾上腺素排泄模式,肾素水平正常的患者比肾素水平低的患者排泄更多肾上腺素(p<0.001)。这些数据与以下概念一致,即在未经治疗的原发性高血压中,PRA可能是肾上腺素能活性的指标,后者是血压对β受体阻滞剂反应的重要决定因素。丁呋洛尔在原发性良性高血压中的降压作用似乎与肾素无关,可能至少部分与外周游离去甲肾上腺素水平降低有关。