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A Hypertension Gene: Are We There Yet?

Published online by Cambridge University Press:  21 February 2012

Samantha J. Lupton
Affiliation:
Unit of Molecular Physiology, School of Medicine, University of Western Sydney, Australia.
Christine L. Chiu
Affiliation:
Unit of Molecular Physiology, School of Medicine, University of Western Sydney, Australia.
Joanne M. Lind*
Affiliation:
Unit of Molecular Physiology, School of Medicine, University of Western Sydney, Australia. j.lind@uws.edu.au
*
*ADDRESS FOR CORRESPONDENCE: Joanne M. Lind, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith NSW 2751, Australia.

Abstract

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Cardiovascular diseases are the leading cause of death worldwide. Essential hypertension is a major risk factor for the development of other cardiovascular diseases and is caused by a combination of environmental and genetic factors, with up to 50% of blood pressure variance currently attributed to an individual's genetic makeup. By studying genes that cause monogenic forms of hypertension and pathways relevant to blood pressure control, a number of polymorphisms have been identified that increase an individual's risk of developing high blood pressure. We report on candidate gene association studies and genome-wide association studies that have been performed to date in the field of hypertension research. It is becoming clear that for the majority of people there is no single gene polymorphism that causes hypertension, but rather a number of common genetic variants, each having a small effect. Using pharmacogenomics to personalize the treatment of hypertension holds promise for achieving and sustaining normotensive pressures quickly, while minimizing the risk of adverse reactions and unwanted side-effects. This will decrease the risk of stroke and myocardial infarction in individuals and lead to a reduced burden of disease upon society as a whole.

Type
Articles
Copyright
Copyright © Cambridge University Press 2011