Mineralocorticoid-Induced Hypertension in Patients with Orthostatic Hypotension

TLDR

The study aimed to investigate the mechanism of recumbent hypertension induced by fludrocortisone in patients with orthostatic hypotension. The authors examined blood‑pressure changes in recumbent and standing positions to elucidate this mechanism. All seven patients showed increased blood pressure in both positions, with hypertensive levels in four; two developed retinopathy and one cardiomegaly; initial elevations were driven by sodium retention and plasma‑volume expansion, but long‑term treatment normalized volume while blood pressure remained high due to increased peripheral vascular resistance, and pressor responsiveness to norepinephrine was enhanced without catecholamine changes.

Abstract

The mechanism of recumbent hypertension induced by fludrocortisone was studied in seven patients with orthostatic hypotension. All showed increases in blood pressure in the recumbent and standing positions, and hypertensive levels were achieved on recumbency in four of them. Hypertensive retinopathy developed in two patients and cardiomegaly in one. Initial blood-pressure elevations were associated with sodium retention and plasma-volume expansion. However, with long-term treatment, plasma volume decreased to control levels despite further blood-pressure increases. Treatment did not affect plasma levels of catecholamines but did enhance pressor responsiveness to infused norepinephrine in some subjects. Hemodynamic studies indicated that hypertension in the recumbent position was related to increases in total peripheral-vascular resistance and not to changes in cardiac output. Clinically, hypertension in the recumbent position is an important risk of fludrocortisone treatment in patients with orthostatic hypotension. This unusual model of chronic mineralocorticoid-induced hypertension is not volume dependent but is related to increased peripheral-vascular resistance.