高血压患者正常血压后代的血管活性体液系统和红细胞中的钠转运。

Physiologia Bohemoslovaca Pub Date : 1990-01-01
V Janata, H Bultasová, P Pinsker
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引用次数: 0

摘要

本文对10例Na(+)-K+共转运活性正常的血压正常者后代和26例高血压家族史阳性的血压正常者的尿钠、钾排泄及影响其转运的一些激素进行了静脉滴注速尿前后的研究。后一组红细胞Na(+)-K+共转运活性分为两个亚组。服用呋塞米后,Na(+)- k +共转运活性降低的Co[-]受试者尿中钠和血管扩张剂(kallikrein、多巴胺、PGE2和前列环素)的排泄量降低。与对照组相比,尿中血管加压因子(PGF2 α、血栓素)的排泄没有变化。Na(+)-K+共转运活性与钾激肽分泌有显著相关性。这些结果表明,在Co[-]受试者中,具有血管舒张或尿钠作用的肾脏物质分泌不足。这可能会对它们的钠排泄产生负面影响。
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Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects.

Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.

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