The primary goals of this study were: 1) Determine the extent to which genetic variability of the RAS genes influenced the distribution of blood pressure (and of RAS intermediate phenotypes) within each population, and contrast the results across populations; 2) Use family studies, within each population, to determine the degree-of familial aggregation of blood pressure, and of the RAS intermediate phenotypes; 3) Use segregation analysis to determine the contribution of 'major genes' to the familial aggregation of blood pressure and of hypertension, and determine whether RAS genes cosegregate with hypertension, or with RAS intermediate phenotypes; 4) Evaluate whether the different prevalence of hypertension in each community reflected differences in their genetic background. The study sites included Ibadan, Nigeria, Kingston, Jamaica, and Maywood, IL. At each site, genetic and epidemiological data were collected from individuals, sampled as follows: individuals comprising 100 five- member structured family sets (proband, spouse, two sibs, one offspring, or half-sib), equally ascertained from the highest and lowest quartiles of the blood pressure distribution, as defined by an ongoing community-wide survey; unrelated singletons, also sampled equally from the highest and lowest blood pressure quartiles. The following measurements were obtained from all participants. Epidemiological variables: blood pressure, height, weight, waist/hip ratio, skinfolds, urine sodium/potassium and sociodemographic variables; Intermediate phenotypes: Plasma levels of angiotensinogen, renin and angiotensin-converting enzyme (ACE); Genotypes: A set of DNA polymorphisms at the four main RAS loci (angiotensinogen, renin, ACE and the angiotensin II-type l receptor).