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膳食钾对原发性高血压患者血流动力学及血浆去甲肾上腺素动力学的影响。

Effects of dietary potassium on the hemodynamics and plasma norepinephrine kinetics in patients with essential hypertension.

作者信息

Ohashi H, Miura Y, Kimura S, Ishizuka Y, Sugawara T, Toriyabe S, Noshiro T, Takahashi M, Sano N, Watanabe H

出版信息

Jpn Circ J. 1985 Sep;49(9):1019-27. doi: 10.1253/jcj.49.1019.

DOI:10.1253/jcj.49.1019
PMID:4068199
Abstract

The effects of dietary potassium on the hemodynamics and plasma norepinephrine (NE) kinetics were studied in 10 patients with borderline hypertension. Potassium supplement (96 mEq daily for 5-7 days) induced a significant (p less than 0.05) fall in blood pressure and a slight decrease in cardiac output. Both urine volume and urinary sodium excretion increased significantly (p less than 0.05) for a first few days following the potassium supplement. The baseline values of the half-time of the rapid NE removal from plasma was significantly delayed in the hypertensive patients (1.05 +/- 0.06 min, p less than 0.05) when compared with those (0.88 +/- 0.04) in normal controls. Potassium supplement induced a significant rise in both plasma NE levels and NE outflow rate (p less than 0.01) in the hypertensive patients, while their half-times were significantly shortened (0.89 +/- 0.07 min, p less than 0.01). The pressor responsiveness to exogenously infused NE tended to diminish during the potassium supplement. These findings indicate that a high potassium intake might accelerate the slowed neuronal NE uptake in the hypertensive patients, while a potassium-induced fall in blood pressure might exert a baroreflex stimulation of NE release. As a net result, an increased NE outflow into the circulation has been confirmed. It is likely that a natriuresis-induced volume contraction might be a predominant factor responsible for the early reduction of blood pressure during the high potassium intake.

摘要

对10例临界高血压患者研究了膳食钾对血流动力学和血浆去甲肾上腺素(NE)动力学的影响。补充钾(每日96毫当量,持续5 - 7天)导致血压显著下降(p < 0.05),心输出量略有降低。补充钾后的最初几天,尿量和尿钠排泄均显著增加(p < 0.05)。与正常对照组(0.88 ± 0.04分钟)相比,高血压患者血浆中NE快速清除半衰期的基线值显著延迟(1.05 ± 0.06分钟,p < 0.05)。补充钾使高血压患者的血浆NE水平和NE流出率均显著升高(p < 0.01),而其半衰期显著缩短(0.89 ± 0.07分钟,p < 0.01)。在补充钾期间,对外源性输注NE的升压反应性趋于减弱。这些发现表明,高钾摄入可能会加速高血压患者神经元对NE摄取的减慢,而钾诱导的血压下降可能会对NE释放产生压力反射刺激。最终结果是,已证实进入循环的NE流出增加。钠利尿诱导的容量收缩可能是高钾摄入期间血压早期降低的主要因素。

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