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(Hypertension. 1998;32:1104-1105.)
© 1998 American Heart Association, Inc.

Letters to the Editor

Concordant Genetic and Physiological Data Are Required for Candidate Genes

John P. Rapp

Department of Physiology and Molecular Medicine Medical College of Ohio, Toledo, Ohio

To the Editor:

In a recent article, Chen et al¹ present additional data on differences in the biochemical and physiological properties of the inducible form of nitric oxide synthase (NOS2) between Dahl salt-sensitive (S) and Dahl salt-resistant (R) rats. The data establish that the enzyme responds differently to increasing concentrations of L-arginine with regard to nitrite production, such that the S enzyme is less active at a given substrate concentration than the R enzyme. This makes sense as a potential mechanism for hypertension in S rats, which would be expected to produce less NO. Also, there was a single base change in the coding region of NOS2, resulting in an amino acid substitution and a DNA restriction fragment length polymorphism (RFLP); this RFLP appeared to be unique to S rats among the several strains tested.

The question arises as to the causative relationship between the above interesting changes and blood pressure differences between S and R rats. In the last paragraph of their article, Chen et al provide a rather misguided attempt to reconcile their biochemical/physiological data with our genetic data.

Chen et al quote our early genetic linkage data² using F₂ populations derived by crossing S with Wistar-Kyoto rats (WKY) or crossing S with the Milan normotensive strain (MNS) that localizes a blood pressure quantitative trait locus (BP QTL) to a region of rat chromosome 10. This region does include NOS2 and did initially support NOS2 as a locus causing inherited differences in blood pressure. Subsequent data using . . . [Full Text of this Article]

Paul W. Sanders; Pei-Yan Chen; Reginald D. Gladish

Nephrology Research and Training Center, Comprehensive Cancer Center and Cell Adhesion and Matrix Research Center, Division of Nephrology, Department of Medicine, Department of Physiology and Biophysics, University of Alabama at Birmingham, Department of Veterans Affairs Medical Center, Birmingham, Ala