Converting-enzyme inhibition corrects the altered adrenal response to angiotensin II in essential hypertension.
Converting-enzyme inhibition corrects the altered adrenal response to angiotensin II in essential hypertension.
复制标题
转化酶抑制可纠正原发性高血压中肾上腺对血管紧张素 II 的反应改变。
DOI：
10.1161/01.hyp.6.1.92
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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：
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作者：
Taylor,T;Moore,TJ;Hollenberg,NK;Williams,GH
在原发性高血压患者中，30%至50%的患者不会随着钠摄入量的变化而调节肾上腺和肾血管对血管紧张素II(AII)的反应。为了明确AII在介导这些改变反应中的作用，我们对31例高血压病患者和13名正常血压对照组在转换酶抑制72小时前和72小时后，分别在钠限制摄入量下观察了AII(0.3，1.0，3.0 ng/kg/min)对肾上腺和肾血管的反应。40%的高血压患者对AII的肾上腺反应低于正常。正常反应组与异常反应组在多项临床和生化指标上无明显差异，但“异常反应组”较“正常反应组”控制AII水平(37+/-3pg/ml比29+/-3pg/ml)显著升高(p<0.03)，而对照血浆醛固酮水平(14+/-2vs22+/-3 ng/dl)降低(P<0.05)。当给予转换酶抑制剂时，正常血压对照组或高血压正常反应者的肾上腺对AII的反应性没有改变。在高血压异常反应者中，短期转换酶抑制后，阈值敏感性和整个剂量反应曲线均显著增强(p<0.01)。这种敏感性的增加不能用AII输注后AII的增加、基础醛固酮水平、血压或基础AII对转换酶抑制的反应的差异来解释。因为无论使用卡托普利还是依那普利(MK 421)，这种现象都会发生，这种现象很可能是转换酶抑制的一种特殊效果。
Of patients with essential hypertension, 30% to 50% do not modulate adrenal and renovascular responsiveness to angiotensin II (AII) with changes in sodium intake. To define the role of AII in mediating these altered responses, the adrenal and renal vascular responses to AII infusion (0.3, 1.0, 3.0 ng/kg/min) were assessed on a sodium-restricted intake in 31 patients with essential hypertension and 13 normotensive controls before and after 72 hours of converting-enzyme inhibition. Forty percent of the hypertensive patients had a subnormal adrenal response to AII. There were no differences between the normal and abnormal responding hypertensive patients in a number of clinical and biochemical factors except that the "abnormal responders" had a significantly (p less than 0.03) greater control AII level (37 +/- 3 vs 29 +/- 3 pg/ml) and lower control plasma aldosterone level (14 +/- 2 vs 22 +/- 3 ng/dl) than the "normal responders." When a converting-enzyme inhibitor was administered, no change in adrenal responsiveness to AII occurred in the normotensive controls or the hypertensive normal responders. In the hypertensive abnormal responders, both the threshold sensitivity and the entire dose response curve was significantly (p less than 0.01) enhanced following short-term converting-enzyme inhibition. This increased sensitivity could not be explained by differences in AII increment with AII infusions, in basal aldosterone levels, or in blood pressure or basal AII response to converting-enzyme inhibition. Since they occurred whether captopril or enalapril (MK 421) were used, this phenomenon is likely to be a specific effect of converting-enzyme inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)