Pratt J H, Luft F C
J Lab Clin Med. 1979 May;93(5):724-9.
The effect of sodium intake on aldosterone production was examined in eight healthy men whose urinary sodium excretion approached their dietary sodium intake at levels of 10, 300, 800 and 1500 mEq sodium/day. Aldosterone secretion was estimated from the excretion rate of two aldosterone metabolites: Thaldo and aldosterone-18-glucuronide. Maximal suppression of aldosterone secretion appeared to have been reached when sodium intake was 800 mEq/day, since no further decrease in aldosteron metabolite excretion rates was observed at 1500 mEq/day dietary sodium. Both plasma renin activity and plasma aldosterone concentration were suppressed and approached or were below the detection limits of the respective radioimmunoassays when sodium intake reached 800 and 1500 mEq/day. Body weight and blood pressure significantly increased at each increment of sodium intake. Our findings show that when sodium intake is extremely high, aldosterone secretion does not decrease to zero but continues at a rate we estimate to be 10 to 30 microgram/day. We suggest that this nonsuppressible secretion of aldosterone may have contributed to the observed increases in weight and blood pressure.
在8名健康男性中研究了钠摄入量对醛固酮生成的影响,这些男性的尿钠排泄量接近其饮食钠摄入量,饮食钠水平分别为每天10、300、800和1500 mEq。醛固酮分泌是根据两种醛固酮代谢物的排泄率来估计的:四氢醛固酮和醛固酮-18-葡萄糖醛酸苷。当钠摄入量为每天800 mEq时,醛固酮分泌似乎已达到最大抑制,因为在饮食钠摄入量为每天1500 mEq时,未观察到醛固酮代谢物排泄率进一步降低。当钠摄入量达到每天800和1500 mEq时,血浆肾素活性和血浆醛固酮浓度均受到抑制,接近或低于各自放射免疫测定的检测限。随着钠摄入量的每次增加,体重和血压显著升高。我们的研究结果表明,当钠摄入量极高时,醛固酮分泌不会降至零,而是以我们估计为每天10至30微克的速率持续分泌。我们认为,醛固酮这种不可抑制的分泌可能导致了观察到的体重和血压升高。