Adrenergic Nervous System in Sodium Metabolism: Effects of Guanethidine and Sodium-retaining Steroids in Normal Man.

Increased activity of the sympathetic nervous system (SNS) has been thought to be partly responsible for sodium retention in congestive heart failure, since sympatholytic drugs may increase the renal excretion of sodium in dogs (1) and patients (2) with congestive heart failure. Two other observations support the suggestion that changes in adrenergic activity may produce changes in renal function. Infusions of norepinephrine, the neurohumoral transmitter of the SNS, can decrease the excretion of sodium in normal subjects and in patients with Addison's disease (3). Patients with autonomic insufficiency excrete sodium at supranormal rates during infusions of normal saline (4). In the present investigation, sodium excretion during infusion of saline and during the administration of a sodium-retaining steroid has been studied before andi after sympathetic blockade by guanethidine. The results of these studies provide additional evidence for a role of the SNS in sodium metabolism.