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原发性高血压男性患者的尿激肽释放酶与盐敏感性

Urinary kallikrein and salt sensitivity in essential hypertensive males.

作者信息

Ferri C, Bellini C, Carlomagno A, Perrone A, Santucci A

机构信息

Institute of I Clinica Medica, Andrea Cesalpino Foundation, University La Sapienza, Rome, Italy.

出版信息

Kidney Int. 1994 Sep;46(3):780-8. doi: 10.1038/ki.1994.333.

DOI:10.1038/ki.1994.333
PMID:7996800
Abstract

A strong influence of urinary kallikrein excretion on the salt sensitivity of blood pressure has been recently suggested in normotensive patients. To evaluate the relationship between kallikrein and salt sensitivity in essential hypertension, active kallikrein excretion, plasma renin activity, atrial natriuretic peptide and aldosterone levels were evaluated in 37 male hypertensives (mean age 43.3 +/- 4.7 years) after two weeks on a normal NaCl diet (120 mmol NaCl per day). After kallikrein determination, salt sensitivity was assessed in a randomized cross-over double-blind fashion by evaluating the blood pressure response to a high (240 mmol NaCl per day for two weeks) and a low (40 mmol NaCl per day for 2 weeks) NaCl intake. Blood pressure changes were evaluated considering as baseline blood pressure the measurement taken at the end of the 2 weeks under normal NaCl intake. Patients were classified as salt sensitive when a diastolic blood pressure change of 10 mm Hg or more occurred after both periods of low and high NaCl intake. At the end of the assessment of salt sensitivity, 19 hypertensive patients (mean age 43.0 +/- 4.6 years) were resistant. The urinary excretion of active kallikrein was significantly lower (P < 0.0001) in salt sensitive (0.51 +/- 0.36 U/24 hr) than in salt resistant patients (1.28 +/- 0.48 U/24 hr). Also, plasma atrial natriuretic peptide levels were higher in salt sensitive than in salt resistant hypertensives (P < 0.02), and a significant correlation between urinary kallikrein and plasma atrial natriuretic peptide was demonstrated in salt sensitive hypertensives (r = -0.691, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

最近有研究表明,在血压正常的患者中,尿激肽释放酶排泄对血压盐敏感性有显著影响。为了评估原发性高血压患者中激肽释放酶与盐敏感性之间的关系,我们对37名男性高血压患者(平均年龄43.3±4.7岁)进行了研究。这些患者在正常氯化钠饮食(每天120 mmol氯化钠)两周后,测定了活性激肽释放酶排泄、血浆肾素活性、心房利钠肽和醛固酮水平。在测定激肽释放酶后,通过评估高盐(每天240 mmol氯化钠,持续两周)和低盐(每天40 mmol氯化钠,持续两周)摄入时的血压反应,以随机交叉双盲方式评估盐敏感性。血压变化以正常氯化钠摄入两周结束时的测量值作为基线血压进行评估。当低盐和高盐摄入期后舒张压变化均达到10 mmHg或更高时,患者被分类为盐敏感。在盐敏感性评估结束时,19名高血压患者(平均年龄43.0±4.6岁)为盐抵抗。盐敏感患者(0.51±0.36 U/24小时)的活性激肽释放酶尿排泄量显著低于盐抵抗患者(1.28±0.48 U/24小时)(P<0.0001)。此外,盐敏感高血压患者的血浆心房利钠肽水平高于盐抵抗患者(P<0.02),并且在盐敏感高血压患者中,尿激肽释放酶与血浆心房利钠肽之间存在显著相关性(r=-0.691,P<0.001)。(摘要截断于250字)

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