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(Hypertension. 2003;41:197.)
© 2003 American Heart Association, Inc.

Editorial Commentary

Loosening the Cuff

Important New Advances in Modeling Antihypertensive Treatment Effects in Genetic Studies of Hypertension

Lyle J. Palmer

From the Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass; and Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio.

Correspondence to Dr Lyle Palmer, Channing Laboratory, Brigham and Women’s Hospital and Harvard, Medical School, 181 Longwood Avenue, Boston MA 02115. E-mail lyle.palmer@channing.harvard.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Human hypertension is a common, chronic disease associated with serious cardiovascular and renal co-morbidity and with substantial social and economic costs. It is therefore important to understand the genetic basis of this disease. The investigation of genetic determinants, and particularly the search for specific susceptibility loci, is likely to be essential to the understanding of disease pathogenesis. Identification of specific genes regulating variation in blood pressure will allow fundamental insights into the pathogenesis of hypertension and will in turn help to better define epidemiological risk factors. The characterization of major genes modulating risk of hypertension and the consequent derivation of improved risk estimation will assist in building the foundation for long-term programs of epidemiological and clinical investigation and intervention. Progress toward these goals holds the potential for enormous public health benefits.¹

The study of familial aggregation is the first step in investigating the genetic basis of any disease. Description of familial aggregation of the disease state and associated phenotypes provides circumstantial evidence for a genetic component to etiology and paves the way for extended genetic investigations. Variance components analysis, the engine for the descriptive genetic epidemiology of quantitative traits, attempts to partition observed variation in a quantitative trait into genetic and nongenetic components.² Variance components analysis, such as that undertaken by Cui et al, is an essential tool in phenotype definition and in exploring the complex pathogenic pathways leading to disease.^3–5 Variance components models can easily be extended to genotype-phenotype analyses and form the basis for several linkage methods.^6,7

	Challenge of Mapping Susceptibility Loci for Hypertension

 
Mapping . . . [Full Text of this Article]

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