本態性高血圧症における尿中Aldosterone排泄について

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With a view of investigating the possibility of augmented or altered.mineralocorticoid activity in essential hypertension, the excretion of aldosterone in hypertensive patients was compared with that of normotensive subjects in various clinical and experimental conditions with simultaneous measurement of urinary electrolytes and of urinary total 17-OHCS. A method for determination of urinary aldosterone was presented. A 24 hour sample of urine was acid-hydrolyzed and extracted with chloroform. After purification of the crude extract by benzene-water partition and column chromatography on florisil gel, the aldosterone was isolated by double chromatographic technique, first in Mattox's formamide-butyl acetate-water system, second in Bush B5, system of benzene-methanol-water and measured by the blue tetrazolium reaction. The simplicity and specificity of the procedure was proved to be generally satisfactory for clinical use. Under basal condition of dietary sodium intake of 290 mEq per day, the sodium excretion became lower along with the elevation of blood pressure. Some of the hypertensive patients seemed to have slightly increased excretion of aldosterone when compared with normotensive subjects. The difference, however, was of questionable statistical significance. Furthermore the values of urinary aldosterone had no correlation with their respective sodium output in urine. No differences in urinary potassium and 17-OHCS were observed between hypertensive patients and normotensive subjects. Following an infusion of 500 ml of 4% sodium chloride, hypertensive patients responded with marked and persistent water diuresis and natriuresis than did normotensive subjects. The fall of aldosterone excretion was apparently limited in the hypertensive group. The response of urinary potassium and of urinary 17-OHCS was similar to that of normotensive subjects. During the restriction of sodium intake of 25 rnEq per day, the patients with slight or moderate hypertension had enhanced sodium conservation capacity with more pronounced increase of aldosterone excretion. But the pattern of response to sodium restriction showed wide individual variation and the quantitative inverse relationship did not exist between sodium excreted in urine and urinary aldosterone level. In hypertensive patients in the advanced stage, these responses were rather impaired. The urinary potassium and 17-OHCS did not change consistently. Although the definite hyperaldosteronism in essential hypertension could not be established, it may be plausible to say that there is some difference in the adaptive response of aldosterone excretion between normotensive and hypertensive subjects.
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本態性高血圧症における尿中Aldosterone排泄について

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