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[原发性高血压患者肾对急性容量负荷反应中利钠肽与肾素-血管紧张素-醛固酮系统的关系]

[Relation between atrial natriuretic factor and the renin-angiotensin-aldosterone system in the renal reaction to acute volume loading in patients with essential hypertension].

作者信息

Horký K, Srámková J, Gregorová I, Dvoráková J

出版信息

Cas Lek Cesk. 1989 Mar 17;128(12):363-7.

PMID:2525071
Abstract

Investigation of changes of the atrial natriuretic factor plasma concentration (ANF), plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) and their correlation with the renal excretion of urine, sodium and potassium before and after infusion of 2 1 saline in the course of 2 hours in 6 controls and 7 patients with essential hypertension (EH) revealed the same rise of ANF in plasma of both groups (from 2.98 +/- 0.45 to 12.36 +/- 1.74 pmol/l in controls and from 3.80 +/- 0.72 to 15.78 +/- 2.06 pmol/l in EH), a comparable decline of PRA (from 0.91 +/- 0.419 to 0.256 +/- 0.127 nmol/l/hr in controls and from 1.711 +/- 0.324 to 0.714 +/- 0.185 nmol/l/hr in EH), and PAC (from 0.30 +/- 0.07 to 0.14 +/- 0.03 nmol/l in controls and from 0.53 +/- 0.13 to 0.24 +/- 0.06 nmol/l in EH). The comparable rise of plasma ANF concentration during infusion of saline was associated with a significantly higher renal excretion of urine and sodium in EH, as compared with controls. The authors conclude from these results that the ANF release into the blood stream after an acute volume overload in EH does not differ from controls. Thus the raised natriuresis in EH after a volume overload cannot be explained solely by the rise of ANF. Its renal action depends obviously on the interaction with many other haemodynamic and renal mechanisms, and as regards humoral factors, in particular on the interaction with the renin-angiotensin-aldosterone system. The inhibitory action of elevated ANF concentrations might participate in the suppression of PRA and PAC after a volume overload.

摘要

对6名对照者和7名原发性高血压(EH)患者在2小时内输注2升生理盐水前后的血浆心房利钠因子浓度(ANF)、血浆肾素活性(PRA)和血浆醛固酮浓度(PAC)变化及其与尿、钠和钾肾排泄的相关性进行研究,结果显示两组血浆ANF均有相同程度升高(对照组从2.98±0.45升至12.36±1.74 pmol/l,EH组从3.80±0.72升至15.78±2.06 pmol/l),PRA有类似下降(对照组从0.91±0.419降至0.256±0.127 nmol/l/hr,EH组从1.711±0.324降至0.714±0.185 nmol/l/hr),PAC也有类似下降(对照组从0.30±0.07降至0.14±0.03 nmol/l,EH组从0.53±0.13降至0.24±0.06 nmol/l)。与对照组相比,EH组在输注生理盐水期间血浆ANF浓度的类似升高与显著更高的尿和钠肾排泄相关。作者从这些结果得出结论,EH患者急性容量超负荷后ANF释放到血流中的情况与对照组无差异。因此,EH患者容量超负荷后钠利尿增加不能仅用ANF升高来解释。其肾脏作用显然取决于与许多其他血液动力学和肾脏机制的相互作用,就体液因素而言,尤其取决于与肾素 - 血管紧张素 - 醛固酮系统的相互作用。升高的ANF浓度的抑制作用可能参与容量超负荷后PRA和PAC的抑制。

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