Fritschka E, Gotzen R, Kittler R, Schöneshöfer M
Br J Pharmacol. 1984 Feb;81(2):245-53. doi: 10.1111/j.1476-5381.1984.tb10071.x.
Treatment of fifteen patients with essential hypertension over four weeks using the beta 1-adrenoceptor blocking agent, metoprolol, resulted in a decrease in 24 h urinary excretion of kallikrein and aldosterone along with a decrease in plasma renin activity. There was no significant change in 24 h excretion rates of the free adrenal steroids deoxycorticosterone, 18-OH-deoxycorticosterone, corticosterone, cortisol or 18-OH-corticosterone during treatment, which were not significantly different from excretion rates of normal males, thus excluding inhibitory effects of adrenal steroids on urinary kallikrein activity. A positive correlation was found between plasma renin activity and urinary excretion of kallikrein during the control period and after 2 weeks on metoprolol, supporting the assumption of a preserved link between the renin-angiotensin-aldosterone system and the renal excretion of kallikrein in these patients. The decrease in kallikrein excretion during beta 1-adrenoceptor blockade in patients with essential hypertension may be explained by a reduction in sympathetic tone and by reduced activity of the renin-aldosterone system.
使用β1 - 肾上腺素能受体阻滞剂美托洛尔对15例原发性高血压患者进行为期四周的治疗,结果显示24小时尿激肽释放酶和醛固酮排泄量减少,同时血浆肾素活性降低。治疗期间,游离肾上腺类固醇脱氧皮质酮、18 - 羟基脱氧皮质酮、皮质酮、皮质醇或18 - 羟基皮质酮的24小时排泄率无显著变化,且与正常男性的排泄率无显著差异,因此排除了肾上腺类固醇对尿激肽释放酶活性的抑制作用。在对照期以及使用美托洛尔治疗2周后,血浆肾素活性与尿激肽释放酶排泄量之间发现正相关,支持了这些患者中肾素 - 血管紧张素 - 醛固酮系统与尿激肽释放酶肾排泄之间存在保留联系的假设。原发性高血压患者在β1 - 肾上腺素能受体阻滞期间激肽释放酶排泄减少,可能是由于交感神经张力降低以及肾素 - 醛固酮系统活性降低所致。