From the Nephrology Research and Training Center, Comprehensive Cancer
Center, and Cell Adhesion and Matrix Research Center, Division of Nephrology,
Department of Medicine, and Department of Physiology, University of Alabama at
Birmingham, and the Department of Veterans Affairs Medical Center, Birmingham,
Ala.
Abstract—Salt-sensitive hypertension
in the Dahl/Rapp rat (S strain) is prevented by L-arginine.
Based on the observations that dexamethasone prevented the
antihypertensive effect of L-arginine in these animals and
the suggestion that a locus in or near an inducible nitric oxide
synthase (NOS) gene on chromosome 10 cosegregated with hypertension in
some F2 crosses that utilized the S rat, the present study explored
the hypothesis that the vascular smooth muscle isoform of inducible NOS
(NOS2) was abnormal in S rats. Primary cultures of aortic smooth muscle
cells from S rats demonstrated impaired inducible NO
production, which improved with increased
L-arginine in the medium. Sequence analysis
identified a single T
© 1998 American Heart Association, Inc.
Scientific Contributions
Vascular Smooth Muscle Nitric Oxide Synthase Anomalies in Dahl/Rapp Salt-Sensitive Rats
C transversion that produced an amino acid
substitution (S714P) between the FAD and FMN binding sites and a
restriction fragment length polymorphism. This restriction fragment
length polymorphism was present only in S rats. The mutation of
NOS2 and the role of this enzyme in the pathogenesis of salt-sensitive
hypertension in the Dahl/Rapp rat require further investigation.
Key Words: : • endothelium-derived relaxing factor • genetics • genes • arginine • vasodilation
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