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(Circulation Research. 2001;89:292.)
© 2001 American Heart Association, Inc.

Editorial

Salt-Sensitive Hypertension and Inducible Nitric Oxide Synthase

Form-Function Dichotomy of a Coding Region Mutation, Mutatis Mutandis

Joseph Loscalzo

From the Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass.

Correspondence to Joseph Loscalzo, MD, PhD, Whitaker Cardiovascular Institute, Boston University School of Medicine, 88 E Newton St, Boston, MA 02118-2394. E-mail jloscalz@bu.edu

Key Words: salt • nitric oxide • nitric oxide synthase • kidney • L-arginine

The earliest recorded association of dietary salt with blood pressure was reported by Huang Ti Nei Ching Su Wein (ca. 1500 B.C.), who noted that "if large amounts of salt are taken, the pulse will stiffen or harden" (page 82).¹ In 1904, Ambard and Beaujard first demonstrated rigorously that dietary salt can increase blood pressure in normal volunteers.² Throughout the 20th century, the relationship between dietary salt and essential hypertension has been debated; however, evolving epidemiological data³ and recent evidence in nonhuman primates,⁴ coupled with a growing understanding of the molecular determinants of sodium handling, clearly support the view that certain individuals defined as salt-sensitive⁵ have a propensity to hypertension when exposed to dietary salt. It is estimated that 50% to 75% of hypertensives are salt-sensitive.⁵

In the 1960s, Dahl first showed that the hypertensive response to salt was genetically determined.⁶ He developed two strains of inbred rat, a salt-sensitive (Dahl S) strain in which blood pressure increased in response to dietary salt and a salt-resistant (Dahl R) strain in which blood pressure did not increase in response to dietary salt. These rats have served as the basis for many genetic studies of salt-sensitive hypertension and its end-organ sequelae for many years; yet, until recently, the molecular basis for this genetic sensitivity remained unknown.

In this issue of Circulation Research, Ying et al⁷ provide functional genetic evidence for the molecular basis of salt sensitivity in this animal model. They identified a mutation in the coding sequence of the inducible . . . [Full Text of this Article]

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