Orthostatic hypotension. Treatment with sodium chloride and sodium retaining steroid hormones

Sodium metabolism, aldosterone excretion, and response to salt and salt-retaining steroid hormones were studied in six patients with orthostatic hypotension. One patient demonstrated definite, and three others minimal, renal salt wasting; two conserved sodium normally. Aldosterone excretion was normal in two patients and reduced in one. Treatment response did not correlate with renal salt wasting or aldosterone excretion. Improvement with treatment correlated with positive sodium balance and weight gain. Dietary sodium restriction blocked the steroid effect, indicating salt and steroids acted mainly through sodium and water retention. Other data in two subjects suggested the salt-retaining hormones may have had an additional effect. Blood pressure diminished in each patient during dietary sodium deprivation and increased with salt administration. Fludrocortisone (Florinef) acetate, given with salt, consistently increased blood pressure further. Thus, full benefit from steroid therapy in these patients required attention to dietary sodium intake.