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 (6-10 g/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.