Myers M G
Clin Pharmacol Ther. 1984 Jul;36(1):57-63. doi: 10.1038/clpt.1984.139.
Patients on beta-blockers may experience a potentially harmful blood pressure rise after topical alpha-adrenoceptors such as phenylephrine. The presumed mechanism for this enhanced pressor responsiveness is unopposed alpha-adrenoceptor activity. This possibility has been investigated in 12 patients with hypertension by infusing increasing intravenous doses of phenylephrine after 2 wk on propranolol, metoprolol, or placebo within a randomized, double-blind, crossover study design. Mean (+/- SE) phenylephrine doses required to increase systolic blood pressure by 25 mm Hg were 4.8 +/- 0.7, 4.7 +/- 0.8, and 5.3 +/- 0.9 microgram/kg on propranolol, metoprolol, and placebo; these differences are not significant. Baroreceptor-mediated decreases in heart rate during phenylephrine infusion were in the same range, 15.8, 15.6, and 17.4 mm Hg on propranolol, metoprolol, and placebo, over baseline heart rate values. In these 12 patients with hypertension, beta-blockade did not induce any appreciable enhancement of alpha-adrenoceptor activity, suggesting that patients with hypertension who receive beta-blockers do not have enhanced pressor responsiveness.
使用β受体阻滞剂的患者在使用去氧肾上腺素等局部α肾上腺素受体激动剂后,可能会出现潜在有害的血压升高。这种升压反应性增强的推测机制是α肾上腺素受体活性未受拮抗。在一项随机、双盲、交叉研究设计中,对12例高血压患者进行了研究,在给予普萘洛尔、美托洛尔或安慰剂2周后,静脉内递增剂量输注去氧肾上腺素。在普萘洛尔、美托洛尔和安慰剂组,使收缩压升高25 mmHg所需的平均(±标准误)去氧肾上腺素剂量分别为4.8±0.7、4.7±0.8和5.3±0.9微克/千克;这些差异不显著。在去氧肾上腺素输注期间,压力感受器介导的心率下降幅度在同一范围内,普萘洛尔、美托洛尔和安慰剂组相对于基线心率值分别为15.8、15.6和17.4 mmHg。在这12例高血压患者中,β受体阻滞未引起α肾上腺素受体活性的任何明显增强,这表明接受β受体阻滞剂治疗的高血压患者不会出现升压反应性增强。