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原发性高血压和原发性醛固酮增多症患者的尿激肽释放酶排泄及血浆肾素活性

Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism.

作者信息

Lechi A, Covi G, Lechi C, Corgnati A, Arosio E, Zatti M, Scuro L A

出版信息

Clin Sci Mol Med. 1978 Jul;55(1):51-5. doi: 10.1042/cs0550051.

Abstract
  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.
摘要
  1. 在相似条件下,对40名血压正常的对照受试者以及74名年龄匹配的原发性高血压患者进行了24小时尿激肽释放酶排泄量的研究。通过使用肾素-钠指数,将高血压患者分为两个亚组:低肾素性高血压患者和正常肾素性高血压患者。还对6名原发性醛固酮增多症高血压患者进行了尿激肽释放酶测定。2. 正常肾素性和低肾素性原发性高血压患者的尿激肽释放酶均显著降低。原发性醛固酮增多症患者的尿激肽释放酶排泄量非常高。3. 在9名高血压患者中,β-肾上腺素能受体阻断疗法使血浆肾素活性显著降低,但对尿激肽释放酶排泄无显著影响。4. 这些结果支持了低尿激肽释放酶可能是原发性高血压标志物的观点。在某些情况下,其排泄与盐皮质激素浓度呈正相关,但它与肾素-血管紧张素系统无主要关联。

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