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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.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 …

Angiotensinogen Genotype and Blood Pressure Responses to Reduced Dietary NaCl and to Weight Loss