Sodium directly impairs target organ function in hypertension.

PURPOSE OF REVIEW: A large body of epidemiologic evidence has been amassed attesting to the relation of increased salt ingestion to the prevalence of hypertension; however, only a minority of patients with essential hypertension are salt sensitive. This report discusses the hypothesis that salt sensitivity need not be demonstrated exclusively by a marked rise in arterial pressure with salt loading; it may also be manifested by evidence of impaired target organ structure and function. RECENT DEVELOPMENTS: This discussion summarizes the authors' recent experience with the spontaneously hypertensive rat, the best experimental model for naturally occurring hypertension, which demonstrates that salt loading precipitates the common structural and functional cardiac and renal changes associated with long-standing hypertension.
SUMMARY: As a result of salt loading, left ventricular diastolic dysfunction and impaired renal excretory function with massive proteinuria occur. Both are associated with marked ischemia and fibrosis and only a small additional increase in arterial pressure.