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转换酶抑制剂可使原发性高血压患者降低的肾上腺对血管紧张素II的反应性恢复正常。

Converting enzyme inhibitors normalize the reduced adrenal responsiveness to angiotensin II in essential hypertension.

作者信息

Williams G H, Hollenberg N K

出版信息

J Hypertens Suppl. 1984 Dec;2(2):S43-7.

PMID:6100876
Abstract

Forty to fifty percent of patients with essential hypertension are unable to modify their adrenal and renal vascular responses to angiotensin II with changes in sodium intake. These individuals have been termed 'non-modulators'. To define the role of angiotensin II in mediating this abnormality, angiotensin II infusions were performed in 31 sodium-restricted subjects before and after 72 h of converting enzyme (ACE) inhibition. Forty percent of these patients had a reduced adrenal response to angiotensin II. When the ACE inhibitor was given to normotensive subjects or hypertensive modulators no change in adrenal responsiveness to angiotensin II was observed. In contrast, in the non-modulators, short-term ACE inhibition significantly enhanced the angiotensin II dose-response curve (P less than 0.01). In a subset of five non-modulators, a third angiotensin II infusion was performed 6-8 weeks after starting the ACE inhibitor. A further enhancement of the adrenal response to angiotensin II was observed at this time point. There was no discernible difference between the response of the non-modulators and the modulating essential hypertensive patients or normotensive controls. Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor.

摘要

40%至50%的原发性高血压患者无法通过改变钠摄入量来调节其肾上腺和肾血管对血管紧张素II的反应。这些个体被称为“非调节者”。为了确定血管紧张素II在介导这种异常中的作用,在31名限钠受试者中,于血管紧张素转换酶(ACE)抑制72小时前后进行了血管紧张素II输注。这些患者中有40%对血管紧张素II的肾上腺反应减弱。当给血压正常的受试者或高血压调节者使用ACE抑制剂时,未观察到肾上腺对血管紧张素II反应性的变化。相反,在非调节者中,短期ACE抑制显著增强了血管紧张素II的剂量反应曲线(P<0.01)。在五名非调节者的一个亚组中,在开始使用ACE抑制剂6至8周后进行了第三次血管紧张素II输注。此时观察到肾上腺对血管紧张素II的反应进一步增强。非调节者与调节性原发性高血压患者或血压正常对照组的反应之间没有明显差异。因此,在近一半的原发性高血压患者中,ACE抑制似乎纠正了钠介导的肾上腺对血管紧张素II反应调节的异常,这表明这种异常反映了血管紧张素II与其受体相互作用的改变。

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