Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: evidence for 18-hydroxycorticosterone to be a better marker than aldosterone.

Abstract

The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticosterone (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8 +/- 0.4 ng AI/ml . h (SD) to 3.4 +/- 1.4 (P less than 0.01), plasma aldosterone from 109 +/- 28 pg/ml to 139 +/- 40 (less than 0.01) and 18-OH-B from 199 +/- 90 to 279 +/- 85 (P less than 0.01). In patients with NREH, PRA increased significantly less (P less than 0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2 +/- 0.1 ng AI/ml . h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111 +/- 37 to 160 +/- 66 (P less than 0.05) and 18-OH-B from 162 +/- 101 to 261 +/- 71 pg/ml (P less than 0.01). The relative increase in plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.