Keusch G, Weidmann P, Ziegler W H, de Châtel R, Reubi F C
Klin Wochenschr. 1980 Jan 2;58(1):25-9. doi: 10.1007/BF01477140.
Plasma catecholamines and renal function were evaluated in 18 patients with essential hypertension treated with the alpha and beta adrenoceptor blocking agent, labetalol. Following 6 weeks of labetalol therapy, blood levels of epinephrine and norepinephrine remained unaltered. Glomerular filtration rate and renal plasma flow were decreased similarly by about 20% (P less than 0.025). Tubular rejection fraction of sodium was increased by 36% (P less than 0.001) while sodium excretion was comparable to control conditions. Labetalol's potential to cause a mild reduction in kidney function should be considered, but may have no clinical consequences in most hypertensive patients receiving such treatment. The lack of increased plasma catecholamine levels during therapy supports the concept that labetalol's alpha-blocking potential is limited to post-junctional receptors, leaving the prejunctional feedback control of catecholamine release intact. Moreover, labetalol's blood pressure-lowering mechanism may be largely independent of changes in sympathetic nervous activity.
对18例接受α和β肾上腺素能受体阻滞剂拉贝洛尔治疗的原发性高血压患者的血浆儿茶酚胺和肾功能进行了评估。拉贝洛尔治疗6周后,肾上腺素和去甲肾上腺素的血药浓度保持不变。肾小球滤过率和肾血浆流量同样降低了约20%(P<0.025)。钠的肾小管重吸收分数增加了36%(P<0.001),而钠排泄与对照情况相当。应考虑拉贝洛尔导致肾功能轻度降低的可能性,但在大多数接受此类治疗的高血压患者中可能没有临床后果。治疗期间血浆儿茶酚胺水平未升高,支持了拉贝洛尔的α阻断作用仅限于节后受体,使儿茶酚胺释放的节前反馈控制保持完整的观点。此外,拉贝洛尔的降压机制可能在很大程度上独立于交感神经活动的变化。