Reduced Aldosterone Excretion in Patients with Autonomic Insufficiency1

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Abstract
Patients with autonomic insufficiency frequently have a reduction in aldosterone excretion that does not respond to stimulation either indirectly by restriction of sodium intake or directly by administration of corticotropin or angiotensin II. Prolonged restriction of sodium intake with concurrent administration of corticotropin and/or angiotensin II eventually effects a modest increase in aldosterone excretion, suggesting chronic absence of an extra-adrenal stimulus to aldosterone production as the probable cause of this reduction rather than an intrinsic adrenal defect. Levels of cortisol were within normal limits in the 5 patients studied and responded promptly to stimulation with corticotropin. The loss of aldosterone responsiveness affects the clinical manifestations of autonomic insufficiency secondarily but at times significantly. During restriction of sodium intake renal conservation of sodium may be inadequate and postural hypotension and weakness increase. Administration of mineralocorticoids can be considered actual replacement therapy for a specific aldosterone deficiency in addition to producing expansion of blood volume by increasing renal retention of sodium, thereby helping to reduce postural hypotension.

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