Genome scans for hypertension and blood pressure regulation.

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Abstract
Interest in the genetic basis of hypertension has spanned the century since it became possible to measure blood pressure (BP). For example, in 1923 Weitz reported several families with a two-generational history of hypertension.1 The nature of the inherited basis of hypertension was the cause of a celebrated debate in the 1950s between Lord Robert Platt and Sir George Pickering.1 Platt argued, based on data such as those of Weitz, that hypertension is a distinct disorder (or a set of such disorders) inherited in a Mendelian fashion. Pickering, while recognizing the importance of inherited factors in BP regulation, argued that these factors operate throughout the range of BP and hypertension simply represents one (arbitrarily defined) extreme of this continuous trait, where by definition BP-raising alleles must aggregate. To some extent both have been proven correct. Several Mendelian forms of hypertension have now been characterized at the molecular level.2 However, these are rare and for the majority of patients with essential hypertension, current data would indicate that any inherited basis of their hypertension is polygenic with complex gene–gene and gene–environment interactions.

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