Velasco M, Guevara J, Morillo J, Ramírez A, Urbina-Quintana A, Hernández-Pieretti O
Br J Clin Pharmacol. 1980 May;9(5):499-504. doi: 10.1111/j.1365-2125.1980.tb05846.x.
The effect of atenolol, a cardioselective β-adrenoceptor acting drug, was studied alone or combined with chlorthalidone on blood pressure, heart rate, systolic time intervals, limb blood flow and limb vascular resistance. Plasma renin activity and plasma atenolol levels were also measured in the study. Supine blood pressure was reduced in group A (11 patients) from 169.4 ± 5.06/111.2 ± 2.63 mmHg to 136.9 ± 2.55/90.9 ± 1.19 mmHg ( < 0.001) during the administration of atenolol alone. Concomitantly supine heart rate was decreased from 83.9 ± 4.10 beats/min to 59.7 ± 1.67 beats/min ( < 0.01) — 4th week. After the administration of atenolol over 8 weeks, supine blood pressure was 138.6 ± 1.21/94.4 ± 2.12 mmHg and supine heart rate was 59.5 ± 2.05 beats/min. Supine blood pressure was reduced in group B (27 patients) from 183.6 ± 4.58/118.7 ± 2.01 mmHg (mean ± s.e. mean of systolic and diastolic blood pressure) to 171.3 ± 4.08/108.9 ± 2.26 mmHg ( < 0.01) during the administration of atenolol alone. Concomitantly supine heart rate was decreased from 84.0 ± 1.89 to 68.7 ± 1.94 ( < 0.001) beats/min. When atenolol was combined with chlorthalidone, supine blood pressure was reduced from 171.3 ± 4.08/108.9 ± 2.26 mmHg to 143.5 ± 3.68/94.8 ± 2.63 mmHg ( < 0.001). Heart rate did not alter significantly with the addition of chlorthalidone. After the administration of atenolol alone in 12 patients of group B, there was a decrease of mean blood pressure from 131.8 ± 2.88 (mean ± s.e. mean) mmHg to 119.0 ± 4.05 mmHg ( < 0.001); of heart rate from 76.4 ± 3.58 beats/min to 57.0 ± 2.55 beats/min ( < 0.001); of calf blood flow from 9.23 ± 1.39 ml 100 g min to 5.05 ± 0.89 ml 100 g min ( < 0.001); and an increase of calf vascular resistance from 16.54 ± 1.90 (mmHg min 100 g)/ml to 28.53 ± 3.40 (mmHg min 100 g)/ml ( < 0.005). Atenolol did not alter significantly pre-ejection period index ( < 0.1). In atenolol-treated patients upon addition of chlorthalidone, there was a further decrease of mean blood pressure from 119.0 ± 4.05 mmHg to 105.9 ± 4.12 mmHg ( < 0.001). There were no further significant alterations of heart rate, pre-ejection period index, calf blood flow, and calf vascular resistance (> 0.01). Atenolol decreased plasma renin activity from 4.69 ± 0.87 to 2.85 ± 0.68 ng ml h ( < 0.05), and chlorthalidone increased it from 2.85 ± 0.68 to 3.81 ± 0.98 ng ml h ( < 0.05). Plasma renin activity on atenolol plus chlorthalidone was not significantly different from that on placebo (> 0.1). There was a 7.8 fold-interindividual variability in the relationship between plasma atenolol concentrations and the atenolol dose upon administration of a single oral dose of 100 mg.
研究了阿替洛尔（一种作用于心脏选择性β - 肾上腺素能受体的药物）单独使用或与氯噻酮联合使用对血压、心率、收缩期时间间期、肢体血流和肢体血管阻力的影响。该研究还测量了血浆肾素活性和血浆阿替洛尔水平。在A组（11例患者）中，单独服用阿替洛尔期间，仰卧位血压从169.4±5.06/111.2±2.63 mmHg降至136.9±2.55/90.9±1.19 mmHg（<0.001）。同时，仰卧位心率在第4周时从83.9±4.10次/分钟降至59.7±1.67次/分钟（<0.01）。服用阿替洛尔8周后，仰卧位血压为138.6±1.21/94.4±2.12 mmHg，仰卧位心率为59.5±2.05次/分钟。在B组（27例患者）中，单独服用阿替洛尔期间，仰卧位血压从183.6±4.58/118.7±2.01 mmHg（收缩压和舒张压的平均值±标准误）降至171.3±4.08/108.9±2.26 mmHg（<0.01）。同时，仰卧位心率从84.0±1.89次/分钟降至68.7±1.94次/分钟（<0.001）。当阿替洛尔与氯噻酮联合使用时，仰卧位血压从171.3±4.08/108.9±2.26 mmHg降至143.5±3.68/94.8±2.63 mmHg（<0.001）。添加氯噻酮后心率无显著变化。在B组的12例患者中，单独服用阿替洛尔后，平均血压从131.8±2.88（平均值±标准误）mmHg降至119.0±4.05 mmHg（<0.001）；心率从76.4±3.58次/分钟降至57.0±2.55次/分钟（<0.001）；小腿血流量从9.23±1.39 ml/100g/min降至5.05±0.89 ml/100g/min（<0.001）；小腿血管阻力从16.54±1.90（mmHg·min/100g）/ml增至28.53±3.40（mmHg·min/100g）/ml（<0.005）。阿替洛尔对射血前期指数无显著影响（<0.1）。在接受阿替洛尔治疗的患者中添加氯噻酮后，平均血压从119.0±4.05 mmHg进一步降至105.9±4.12 mmHg（<0.001）。心率、射血前期指数、小腿血流量和小腿血管阻力无进一步显著变化（>0.01）。阿替洛尔使血浆肾素活性从4.
