Blood pressure regulation in autonomic failure by dietary sodium, blood volume and posture

Abstract

In normal subjects natriuresis is tightly coupled to dietary salt ingestion to maintain sodium balance. Likewise, blood pressure remains unchanged over a wide range of salt intake because of pressure natriuresis, whereby an increase in blood pressure stimulates renal sodium excretion to restore homeostasis. These sodium handling mechanisms are impaired in autonomic failure. When exposed to salt restriction, autonomic failure patients are unable to reduce renal sodium excretion, and their orthostatic hypotension worsens. It follows that increased dietary salt would improve orthostatic tolerance. Indeed, most clinical practice guidelines emphasize a high salt intake (6-10g/day) in the treatment of neurogenic orthostatic hypotension. This approach has been shown to improve other conditions such as syncope and postural tachycardia syndrome, but surprisingly there is no empirical evidence to support this recommendation in orthostatic hypotension. Even though there is expert opinion consensus in its favor, it would be reassuring if at least mechanistic proof of concept studies were available. Fludrocortisone is often added to a high salt diet to improve sodium retention and increase plasma volume, but these effects are transient. Fludrocortisone is contraindicated in patients with heart failure and should be used with caution, if at all, if supine hypertension is present. In patients with supine hypertension posture is an important determinant of sodium balance; blood pressure substantially increases while supine, triggering pressure natriuresis and extensive sodium loss. Thus, avoiding the supine posture may be as important as increasing dietary salt in the management of orthostatic hypotension.