AI Article Synopsis

  • The study investigates the causes of high blood pressure in two conditions: primary aldosteronism and low-renin essential hypertension, linking both to mineralocorticoid excess.
  • The research shows that while primary aldosteronism clearly involves increased aldosterone leading to high blood pressure, low-renin essential hypertension may be related to an unknown mineralocorticoid despite normal aldosterone levels.
  • During treatment with adrenal inhibitors, both conditions showed blood pressure reduction; however, in low-renin essential hypertension, blood pressure did not significantly change despite a decrease in aldosterone, indicating a likely role of other unidentified mineralocorticoids in this condition.

Article Abstract

The blood pressure elevation of primary aldosteronism is caused by excessive production of the known mineralocorticoid, aldosterone. The blood pressure elevation of low-renin essential hypertension may also be caused by mineralocorticoid excess, but which which mineralocorticoid is responsible is uncertain. Normal levels of aldosterone, found in this disorder despite suppressed plasma renin, and the presence of an unknown mineralocorticoid have been hypothesized to explain low-renin essential hypertension. We contrasted the blood pressure responses and changes in aldosterone seen in patients with low-renin essential hypertension and primary aldosteronism during treatment with two adrenal enzyme inhibitors. The results demonstrate the similarity between decrease in blood pressure and in aldosterone during early adrenal inhibition in both primary aldosteronism and in low-renin essential hypertension. During treatment with a distal adrenal blocker, patients with primary aldosteronism demonstrated decreases in both aldosterone and blood pressure, whereas patients with low-renin essential hypertension showed a decrease in aldosterone without significant change in blood pressure. This suggested that aldosterone was not the major mineralocorticoid responsible for low-renin essential hypertension. Unknown mineralocorticoid excretion decreased (along with blood pressure) during early inhibition but failed to decrease (along with blood pressure) during late inhibition at a time when aldosterone excretion decreased. This suggests that unknown mineralocorticoids play significant roles in the blood pressure elevation of low-renin essential hypertension.

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