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原发性高血压患者输注氯化钠引起的钠排泄增加,同时伴有尿3',5'-环磷酸鸟苷排泄增加。

Exaggerated natriuresis induced by sodium chloride infusion in essential hypertension is accompanied by an exaggerated urinary 3' 5' guanosine monophosphate excretion.

作者信息

Widecka K, Celibała R, Goździk J, Syrenicz A, Ciechanowski K, Czekalski S

机构信息

Department of Endocrinology and Metabolic Diseases, Pomeranian University School of Medicine, Szczecin, Poland.

出版信息

Nephrol Dial Transplant. 1993;8(8):711-5. doi: 10.1093/ndt/8.8.711.

DOI:10.1093/ndt/8.8.711
PMID:8414156
Abstract

The effects of an intravenous infusion of physiological saline on plasma atrial natriuretic peptide (ANP), guanosine 3' 5' monophosphate (cGMP) concentrations, and on urinary cGMP and sodium excretion were studied in 13 patients with essential hypertension, class I according to WHO criteria, and in 10 healthy subjects. It was found that the groups did not differ as to basal and infusion-induced plasma ANP and cGMP and basal urinary cGMP and sodium excretion, but the sodium chloride infusion resulted in a significantly greater urinary cGMP and sodium excretion and creatinine clearance in hypertensive than in control subjects. The results of this study demonstrate that patients with essential hypertension respond to an intravenous sodium chloride load not only with exaggerated natriuresis, but also with augmented urinary cGMP excretion. The latter finding may in part be due to a greater glomerular filtration of cGMP, but increased renal contribution cannot be excluded. Apart from the possible stronger intrarenal effect of ANP on cGMP production in patients with hypertension, independent direct effect of volume expansion on cGMP excretion and modified activity of other cGMP generating systems may all be responsible for the higher urinary cGMP excretion in essential hypertension.

摘要

在13例符合世界卫生组织标准I级的原发性高血压患者和10名健康受试者中,研究了静脉输注生理盐水对血浆心房利钠肽(ANP)、鸟苷3',5'-单磷酸(cGMP)浓度以及尿cGMP和钠排泄的影响。结果发现,两组在基础和输注诱导的血浆ANP和cGMP以及基础尿cGMP和钠排泄方面并无差异,但与对照组相比,输注氯化钠后高血压患者的尿cGMP、钠排泄及肌酐清除率显著更高。本研究结果表明,原发性高血压患者静脉输注氯化钠负荷后不仅会出现钠利尿增强,尿cGMP排泄也会增加。后一发现部分可能是由于cGMP的肾小球滤过增加,但肾脏贡献增加也不能排除。除了ANP对高血压患者cGMP生成可能具有更强的肾内作用外,血容量扩张对cGMP排泄的独立直接作用以及其他cGMP生成系统活性的改变都可能导致原发性高血压患者尿cGMP排泄增加。

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1
Exaggerated natriuresis induced by sodium chloride infusion in essential hypertension is accompanied by an exaggerated urinary 3' 5' guanosine monophosphate excretion.原发性高血压患者输注氯化钠引起的钠排泄增加,同时伴有尿3',5'-环磷酸鸟苷排泄增加。
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引用本文的文献

1
Chamber-specific regulation of atrial natriuretic peptide secretion in cardiac hypertrophy: atrial wall dynamics in the ANP secretion.心脏肥厚中心房利钠肽分泌的腔室特异性调节:ANP 分泌中的心房壁动力学。
Pflugers Arch. 2020 Jun;472(6):639-651. doi: 10.1007/s00424-020-02377-2. Epub 2020 May 2.
2
A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function.一种遗传模型确定了心钠素受体(鸟苷酸环化酶 -A)在肾功能调节中的重要性。
Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4369-73. doi: 10.1073/pnas.97.8.4369.
3
The heart communicates with the kidney exclusively through the guanylyl cyclase-A receptor: acute handling of sodium and water in response to volume expansion.
心脏仅通过鸟苷酸环化酶-A受体与肾脏进行交流:对容量扩张的钠和水的急性处理。
Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6215-9. doi: 10.1073/pnas.93.12.6215.