Ohman K P, Karlberg B E, Nilsson O R, Wettre S
Clin Exp Hypertens A. 1983;5(4):523-9. doi: 10.3109/10641968309081789.
The effects on blood pressure, the renin-angiotensin-aldosterone and the kallikrein-kinin systems were investigated in 32 patients with primary hypertension WHO stage I-II treated with captopril. Hydrochlorothiazide was added if needed to achieve a supine diastolic blood pressure of less than or equal to 90 mmHg. A placebo control group (n=8) was treated similarly. Supine mean arterial pressure fell from 133 +/- 10 on placebo to 114 +/- 12 mmHg after 4 weeks on captopril. At the same time plasma aldosterone decreased from 263 +/- 188 to 164 +/- 101 pmol . 1(-1), 24 h urinary excretion of aldosterone from 18 +/- 12 to 12 +/- 10 nmol and kallikrein from 9.0 +/- 6.7 to 6.2 +/- 4.1 nkat. Plasma angiotensin II was significantly reduced after two weeks treatment from 23.2 +/- 8.6 to 17.0 +/- 6.7 pmol . 1(-1). Before, but not during captopril, 24 h urinary kallikrein excretion correlated with plasma aldosterone levels and 24 h urinary aldosterone excretion (r=0.44 p, less than 0.05 and r=0.53, p less than 0.01, respectively). Mean arterial pressure reduction on captopril correlated with pretreatment PRA (r=0.44, p less than 0.05) but not with other measured hormone levels or changes therein. The addition of hydrochlorothiazide caused a further fall in blood pressure, but increased plasma aldosterone and 24 h urinary kallikrein excretion. Hydrochlorothiazide alone increased only 24 h urinary aldosterone excretion significantly. These findings indicate that, besides aldosterone secretion and renal arterial pressure, further mechanisms regulating the release of and activity of the renal kallikrein-kinin system exist.
对32例世界卫生组织I-II期原发性高血压患者使用卡托普利治疗，研究其对血压、肾素-血管紧张素-醛固酮系统以及激肽释放酶-激肽系统的影响。必要时加用氢氯噻嗪，以使仰卧位舒张压小于或等于90mmHg。设立安慰剂对照组（n = 8），进行类似治疗。服用安慰剂时仰卧位平均动脉压为133±10mmHg，服用卡托普利4周后降至114±12mmHg。同时，血浆醛固酮从263±188降至164±101pmol·1⁻¹，24小时尿醛固酮排泄量从18±12降至12±10nmol，激肽释放酶从9.0±6.7降至6.2±4.1nkat。治疗两周后血浆血管紧张素II显著降低，从23.2±8.6降至17.0±6.7pmol·1⁻¹。在服用卡托普利之前（而非服药期间），24小时尿激肽释放酶排泄量与血浆醛固酮水平以及24小时尿醛固酮排泄量相关（r分别为0.44，p<0.05和r为0.53，p<0.01）。服用卡托普利后平均动脉压的降低与治疗前的肾素活性相关（r = 0.44，p<0.05），但与其他测量的激素水平或其变化无关。加用氢氯噻嗪导致血压进一步下降，但血浆醛固酮和24小时尿激肽释放酶排泄量增加。单独使用氢氯噻嗪仅使24小时尿醛固酮排泄量显著增加。这些发现表明，除醛固酮分泌和肾动脉压外，还存在调节肾激肽释放酶-激肽系统释放和活性的其他机制。
