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尿激肽释放酶排泄的环境决定因素。

Environmental determinants of urinary kallikrein excretion.

作者信息

Hunt S C, Wu L L, Slattery M L, Meikle A W, Williams R R

机构信息

Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City.

出版信息

Am J Hypertens. 1993 Mar;6(3 Pt 1):226-33.

PMID:8466710
Abstract

Decreased urinary kallikrein excretion has been shown to be related to hypertension. Kallikrein levels also have been shown to be determined primarily by genes, with 51% of the total variance being due to a single gene. However, there exists strong spouse-spouse correlation, indicating that common environment plays a significant role. This study used 69 pairs of monozygous twins to investigate possible dietary, biochemical, and anthropometric determinants of kallikrein that could result in this high spouse correlation. Urinary sodium and potassium excretion differences were significantly related to kallikrein differences, with urinary potassium having the strongest relationship (r = 0.46, P = .0001). Urinary pH (r = 0.23, P = .03) and systolic blood pressure (r = -0.25, P = .03) differences were associated with urinary kallikrein excretion differences independently of urinary potassium. Information on nutrients was obtained from a dietary food frequency questionnaire that ascertains usual intake over the last 5 years. Kallikrein differences between monozygous twins were not explained by differences in nutrient intake as measured by this questionnaire. Therefore, urinary potassium and pH probably represent the more acute effects of recent dietary sodium and potassium intake on urinary kallikrein levels. Urinary potassium, pH, and systolic blood pressure differences explained 34% of the difference in kallikrein levels between monozygous twins. The significant difference in systolic blood pressure between twins, even after controlling for electrolyte excretion differences suggests an additional unmeasured environmental variable that is associated with decreased kallikrein excretion and elevated blood pressure.

摘要

尿激肽释放酶排泄减少已被证明与高血压有关。激肽释放酶水平也已被证明主要由基因决定,总变异的51% 归因于单个基因。然而,存在很强的配偶间相关性,这表明共同环境起着重要作用。本研究使用69对同卵双胞胎来调查可能导致这种高配偶相关性的激肽释放酶的饮食、生化和人体测量学决定因素。尿钠和钾排泄差异与激肽释放酶差异显著相关,其中尿钾的相关性最强(r = 0.46,P = .0001)。尿pH值(r = 0.23,P = .03)和收缩压(r = -0.25,P = .03)差异与尿激肽释放酶排泄差异相关,且独立于尿钾。营养信息来自一份饮食频率问卷,该问卷确定过去5年的通常摄入量。同卵双胞胎之间的激肽释放酶差异无法用该问卷测量的营养摄入量差异来解释。因此,尿钾和pH值可能代表近期饮食中钠和钾摄入量对尿激肽释放酶水平的更直接影响。尿钾、pH值和收缩压差异解释了同卵双胞胎之间激肽释放酶水平差异的34%。即使在控制了电解质排泄差异后,双胞胎之间收缩压的显著差异仍表明存在一个未测量的额外环境变量,该变量与激肽释放酶排泄减少和血压升高有关。

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1
Environmental determinants of urinary kallikrein excretion.尿激肽释放酶排泄的环境决定因素。
Am J Hypertens. 1993 Mar;6(3 Pt 1):226-33.
2
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Relationship of urinary sodium/potassium excretion and calcium intake to blood pressure and prevalence of hypertension among older Chinese vegetarians.中国老年素食者尿钠/钾排泄及钙摄入量与血压和高血压患病率的关系
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引用本文的文献

1
Arterial and renal consequences of partial genetic deficiency in tissue kallikrein activity in humans.人类组织激肽释放酶活性部分基因缺陷的动脉和肾脏后果。
J Clin Invest. 2005 Mar;115(3):780-7. doi: 10.1172/JCI23669.
2
Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice.组织激肽释放酶缺陷小鼠中血压正常的心血管异常。
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2634-9. doi: 10.1073/pnas.051619598. Epub 2001 Feb 20.