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(Hypertension. 2007;50:161.)
© 2007 American Heart Association, Inc.

Sixth International Workshop on Structure and Function of the Vascular System

The Salt Conundrum

A Hypothesis

From the Oshsner Clinic Foundation, New Orleans, La.

Correspondence to Edward D. Frohlich, MD, Alton Ochsner Distinguished Scientist, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121. E-mail efrohlich@ochsner.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
For millennia, salt has had an intimate history with human social, economic, and political relationships. In earlier times man’s work value was paid in salt as gauged by body weight, social stature was dictated by assigned position at the table nearest to the salt, and its etymological root still remains in common parlance.¹ Early last century, however, the relationship between salt intake and health was recognized.² Initially, this relationship was made with the association between magnitude of salt intake and hypertension; but more recently two achievements make a major impact on this subject, the quantitative measurement of dietary sodium intake and repeated recognition that the greater the daily sodium intake, the higher the prevalence of hypertension in populations.

	The Problem: A Conundrum

 
The vital importance of the salt-hypertension relationship remains today even though several concerns exist (albeit with some controversy). Thus, despite the direct relationship between salt consumption and prevalence of hypertension in populations, when increased sodium intake of one specific patient exists, arterial pressure may not necessarily increase; and, therefore, establishment of a direct cause–effect clinical relationship has been difficult to fully appreciate. Therefore, to my way of thinking, the term "salt-dependent" hypertension has been inadequate to explain the clinical relationship between salt-loading and response of arterial pressure. Indeed, sodium-dependent hypertension so-defined exists only in about one-third patients with essential hypertension.³ So why is there such close correlation between salt and hypertension?^4,5 Conversely, why has it been so difficult to demonstrate that an individual hypertensive patient is sodium-dependent? What can explain this conundrum? . . . [Full Text of this Article]

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