Captopril enhances vascular and adrenal responsiveness to angiotensin II in essential hypertension.
Captopril enhances vascular and adrenal responsiveness to angiotensin II in essential hypertension.
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卡托普利可增强原发性高血压患者血管和肾上腺对血管紧张素 II 的反应性。
DOI：
10.1042/cs0660299
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Williams,GH
中科院分区：
文献类型：
--
作者：
Koletsky,RJ;Gordon,MB;LeBoff,MS;Moore,TJ;Dluhy,RG;Hollenberg,NK;Williams,GH
1.用转换酶抑制剂卡托普利（25-50 mg，每6 h口服一次，共66 h），对11例肾素正常的原发性高血压患者进行了钠平衡改变与血管紧张素Ⅱ（ANG Ⅱ）水平的分离。在给予卡托普利之前和之后，测量对分级输注ANG II（0.3、1和3 pmol kg− 1 min −1）的升压、肾血管和肾上腺反应。通过测量舒张压（DBP）评估全身血管反应，通过测量对氨基马尿酸（PAH）清除率评估肾血管反应，通过测量血浆醛固酮评估肾上腺反应.高血压患者服用卡托普利66小时后，对ANG Ⅱ的血压反应性显著增强（P<0.004），但对去甲肾上腺素的反应性无显著差异。ANG II（3 pmol kg− 1 min −1）也使卡托普利给药后PAH清除率（−194 ± 40 ml/min）比给药前（− 104 ± 15 ml/min）显著降低（P<0.03）。这些结果表明，这两种靶组织对ANG II的反应性是由循环ANG II水平决定的.在肾上腺中，给予巯甲丙脯酸后（P< 0.01）醛固酮对ANG II的反应也显著高于给予巯甲丙脯酸前（3 pmol kg− 1 min −1时的增量：660 ± 88 vs 381 ± 94 pmol/l）。这些结果与以前报道的血压正常受试者的反应形成鲜明对比，并支持原发性高血压受试者醛固酮分泌调节改变的假设。
1. The converting-enzyme inhibitor captopril (25–50 mg orally every 6 h for 66 h) was used to dissociate the circulating levels of angiotensin II (ANG II) from changes in sodium balance in 11 patients with normal renin essential hypertension on 10 mmol of sodium/day intake. Pressor, renal vascular and adrenal responses to graded infusions of ANG II (0.3, 1 and 3 pmol kg−1min−1) were measured before and after captopril administration. Systemic vascular responses were assessed by measuring diastolic blood presusre (DBP), renovascular responses by measuringp-aminohippurate (PAH) clearance and adrenal responses by measuring plasma aldosterone.2. After receiving captopril for 66 h the hypertensive subjects showed a significantly (P<0.004) enhanced blood pressure response to the infused ANG II but not to noradrenaline when compared with the response before captopril. ANG II (3 pmol kg−1min−1) also produced a significantly (P<0.03) greater reduction in PAH clearance after (−194 ± 40 ml/min) compared with before (−104 ± 15 ml/min) captopril. These results suggest that the responsiveness to ANG II in these two target tissues is determined by the circulating ANG II level.3. In the adrenal gland the aldosterone responses to ANG II also were significantly greater after (P< 0.01) than before captopril (increment at 3 pmol kg−1min−1: 660 ± 88 vs 381 ± 94 pmol/l). These results are in distinct contrast with the responses previously reported for normotensive subjects and support the hypothesis that the regulation of aldosterone secretion is altered in subjects with essential hypertension.