原发性高血压和醛固酮增多症患者尿钾激肽分泌和血浆肾素活性。

A Lechi, G Covi, C Lechi, A Corgnati, E Arosio, M Zatti, L A Scuro
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引用次数: 60

摘要

1. 研究了40名正常血压对照者和74名年龄匹配的原发性高血压患者在相似条件下的24小时尿钾激肽排泄情况。采用肾素钠指数将高血压患者分为低肾素高血压和正常肾素高血压两组。对6例原发性醛固酮增多症高血压患者进行尿钾激肽测定。2. 正常肾素和低肾素原发性高血压患者尿钾激肽显著降低。原发性醛固酮增多症患者尿钾激肽的排泄量非常高。3.在9例高血压患者中,β -肾上腺素受体阻断治疗导致血浆肾素活性显著降低,但对尿钾激肽排泄无显著影响。4. 结果支持尿钾激肽水平低可能是原发性高血压的标志这一概念。在一定条件下,其排泄与矿化皮质激素浓度呈正相关,但与肾素-血管紧张素系统无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism.

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.

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