(Hypertension. 1997;29:918-922.)
© 1997 American Heart Association, Inc.
Articles |
From Duke University Medical Center, Durham, NC (L.P.S., Y.-T.C., L.P.); Louisiana State University Medical Center (S.P.M.), New Orleans; and National Institutes of Health, National Center for Human Genome Research, Baltimore, Md (A.F.W.).
Abstract Salt sensitivity is a heritable trait that is a
hallmark of hypertension in black Americans. Genes encoding adrenergic
receptors are candidate loci for the inheritance of this
hypertension-related trait because of the role of these receptors in
the regulation of renal sodium excretion and vascular tone. We
performed this study to determine whether these loci are responsible
for some of the phenotypic variation in salt sensitivity. Hypertensive
black American probands were ascertained, followed by sequential
ascertainment of adult sib pairs among the first-, second- and
third-degree relatives of the proband. Both hypertensive and
normotensive siblings were tested for salt sensitivity by an
intravenous sodium-loading, lasix volume-depletion protocol. Genotyping
was performed with restriction fragment length polymorphisms in genomic
DNA probed with clones containing the ß2- and
2c10-adrenergic receptor genes. A total of 109 sib pairs
was evaluated. Salt sensitivity was defined as the change in blood
pressure in each individual, comparing the sodium-loaded with the
volume-depleted state. Systolic pressure decreased by an average of
9.0±9%, diastolic pressure by 1.5±11%, and mean arterial pressure
by 5.0±9%. Neither blood pressure nor salt sensitivity was linked at
the
2c10-adrenergic receptor locus. No evidence
suggested that systolic salt sensitivity and baseline blood pressure
were linked at the ß2-adrenergic receptor locus.
Model-independent sib pair linkage analysis suggested that diastolic
blood pressure response to sodium loading/volume depletion is linked at
the ß2-adrenergic receptor locus (P<.006).
Evidence for linkage was significant at the .05 level after adjustment
for the number of phenotypic traits examined.
Key Words: blacks hypertension, genetic genetics sodium
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