Rahn K H, Gierlichs H W, Planz G, Planz R, Schols M, Stephany W
Eur J Clin Invest. 1978 Jun;8(3):143-8. doi: 10.1111/j.1365-2362.1978.tb00827.x.
The influence of the beta receptor blocking agent propranolol on plasma catecholamine concentrations was studied in eight patients with essential hypertension. The study was of single blind crossover design. Propranolol given in oral doses ranging from 60 to 240 mg daily for a period of 3 weeks decreased blood pressure and heart rate. The beta-adrenergic blocking agent caused plasma catecholamine levels to increase both at rest and during bicycle exercise. Chromatographical analysis showed that concentrations of noradrenaline as well as of adrenaline rose during treatment with propranolol. However, dopamine-beta-hydroxylase activity in plasma was not altered. Furthermore, the urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy mandelic acid did not change during beta receptor blockade. The results are compatible with the assumption that antihypertensive doses of propranolol by decreasing cardiac output cause an activation of the sympatho-adrenal system.
在8例原发性高血压患者中研究了β受体阻滞剂普萘洛尔对血浆儿茶酚胺浓度的影响。该研究采用单盲交叉设计。口服剂量为每日60至240毫克的普萘洛尔,持续3周,可降低血压和心率。β肾上腺素能阻滞剂使静息和自行车运动时的血浆儿茶酚胺水平均升高。色谱分析表明,普萘洛尔治疗期间去甲肾上腺素和肾上腺素的浓度均升高。然而,血浆中多巴胺-β-羟化酶的活性未改变。此外,在β受体阻滞期间,去甲肾上腺素、肾上腺素和4-羟基-3-甲氧基扁桃酸的尿排泄量没有变化。这些结果与以下假设相符:降压剂量的普萘洛尔通过降低心输出量导致交感-肾上腺系统激活。