低レニン性本態性高血圧症におけるアルドステロン分泌調節機序に関する研究
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In order to clarify the regulation of aldosterone secretion in low-renin essential hypertension, plasma renin activity and plasma aldosterone were measured before and after an upright position with a furosemide administration in 168 cases of essential hypertension and 5 cases of primary aldosteronism. Essential hypertension was divided into low-, normal- and high-renin groups from the results obtained by this renin stimulating experiment. Plasma cortisol and plasma ACTH were measured before and after the experiment in 40 cases of essential hypertension and in 5 cases of primary aldosteronism. The effects of angiotensin II and ACTH-Z on plasma aldosterone and circulating plasma volume were measured and evaluated using the radio iodine labeled serum albumin method. <BR>In the low-renin group, the upright position with a furosemide administration induced an elevation in plasma aldosterone without a significant change in PRA. However, plasma aldosterone correlated positively with PRA even in the low-renin group (before r=0.507, after r=0.759), but did not correlate with ACTH before and after the experiment. On the other hand, in primary aldosteronism, plasma aldosterone correlated positively with plasma cortisol and ACTH, but it did not correlate with PRA during the experiment. The increase of plasma aldosterone during the angiotensin II administration was lower in the low-renin group and in primary aldosteronism than it was in the normal- or high-renin groups. The increment of plasma aldosterone after ACTH-Z was similar in all groups; however, it was significantly higher in primary aldosteronism than it was in essential hypertension. The circulating plasma volume was similar in all groups except that it was high in primary aldosteronism. <BR>The data indicate that in low-renin essential hypertension, the adrenal receptor is not necessarily sensitive to angiotensin II, and plasma aldosterone change is regulated by the renin-angiotensin system. The syndrome of documented primary mineralocorticoid excess is rare and constitutes a small fraction of low-renin essential hypertension. On the other hand, in primary aldosteronism, the adrenal receptor is not sensitive to angiotensin II, and plasma aldosterone is regulated by an endogeneous ACTH secretion rather than the renin-angiotensin system.
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