From the Department of Medicine, Medical College of Wisconsin
(Milwaukee).
Correspondence to Theodore A. Kotchen, MD, Department of Medicine, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226.
What relevance, if any, these or similar polymorphisms may have to
blood pressure regulation or hypertension in the general population
remains to be determined. Despite evidence for heritability, essential
hypertension is a complex trait that does not exhibit classic mendelian
modes of inheritance attributable to a single gene
locus.2 Multiple genetic loci may be involved in
blood pressure regulation, and hypertension may be related to the
interaction of susceptible genes with environmental stressors, such as
dietary sodium chloride (NaCl) consumption.
Trials of Hypertension Prevention (TOHP) is a longitudinal study
designed to evaluate the efficacy of reduction of dietary NaCl and of
weight loss on blood pressure in a cohort of moderately overweight
adults with diastolic blood pressures of 83 to 89
mm Hg.3 In this issue of
Hypertension, Hunt et al4 report that
© 1998 American Heart Association, Inc.
Scientific Contributions
Editorial Commentary: Angiotensinogen Genotype and Blood Pressure Responses to Reduced Dietary NaCl and to Weight Loss
Key Words: angiotensinogen blood pressure genetics clinical trials Editorial
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Introduction
With the human genome project nearing
completion and with the increasing availability of genotyping
technology, there is considerable interest in identifying genes that
contribute to hypertension and to physiological
determinants of hypertension. In a number of relatively rare
hypertensive disorders, specific genetic polymorphisms resulting in
elevated arterial pressure have recently been described,
eg, glucocorticoid-remediable primary aldosteronism, Liddle's
syndrome, and the syndrome of apparent mineralocorticoid
excess.1 In several but not all of these
disorders, hypertension is the consequence of alterations of either
adrenal steroid metabolism or direct renal tubular function
resulting in antinatriuresis. Conversely, specific polymorphisms
have been identified that result in alterations of renal tubular
function that promote natriuresis and consequently relatively low blood
pressure levels.
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