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钠负荷高血压患者补钾相关的血流动力学和内分泌变化

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

作者信息

Fujita T, Ando K

出版信息

Hypertension. 1984 Mar-Apr;6(2 Pt 1):184-92.

PMID:6373586
Abstract

To clarify the mechanism by which potassium (KCl) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KCl loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KCl supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCl supplement (p less than 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p less than 0.05) or with changes in cardiac output (p less than 0.01). The results suggest that KCl may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p less than 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为阐明钾(氯化钾)预防钠(氯化钠)升高血压作用的机制,我们研究了氯化钾负荷对特发性高血压患者的影响,这些患者在经过一段时间的氯化钠限制后,摄入高氯化钠饮食。11例在高氯化钠阶段服用氯化钾补充剂(96毫当量/天)的患者,当氯化钠摄入量从25毫当量/天增加到250毫当量/天时,其平均血压(MAP)升高幅度小于12例未服用氯化钾补充剂的患者(p<0.001)。高氯化钠饮食时,服用氯化钾补充剂的患者比未服用者保留的氯化钠更少,体重增加更少,血浆容量和心输出量增加幅度也更小。总体而言,高钠饮食期间血压水平的升高与血浆容量变化(p<0.05)或心输出量变化(p<0.01)直接相关。结果表明,氯化钾可能通过减弱心输出量的增加(主要是由于利钠作用)来预防高血压患者因氯化钠负荷导致的血压升高。此外,由于已知交感神经系统控制尿氯化钠排泄,因此测量了血浆去甲肾上腺素以评估交感神经活性。从低氯化钠饮食到高氯化钠饮食的第3天,服用氯化钾补充剂的患者血浆去甲肾上腺素显著降低(p<0.01),而未服用者则保持不变。(摘要截选至250字)

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