Genetics of Hypertension in Blacks

July 11, 2016 updated by: National Heart, Lung, and Blood Institute (NHLBI)
To investigate the genetic determinants of hypertension in three populations of the African diaspora, with a major focus on clarifying the role of genes that code for the renin-angiotensin system (RAS).

Study Overview

Status

Completed

Conditions

Detailed Description

BACKGROUND:

This community-based study in three geographically distinct populations of West African heritage with contrasting levels of hypertension risk was one of the first comprehensive examinations of the genetics of hypertension in African Americans. The study focused on the renin-angiotensin system (RAS) because it was the only physiological arm of blood pressure control for which candidate genes had been securely linked to the risk of hypertension. Polymorphisms at the angiotensinogen locus varied considerably between Blacks and whites. The documented Black:white differences in the RAS system emphasized the importance of determining whether RAS genes contributed to the excessively high risk of hypertension experienced by African Americans. The study generated unique information about the variability of the RAS loci in populations of West African heritage, and the contribution of this variability to hypertension risk. The data from the study, including the DNA specimens, also represented a valuable resource for future work on the genetics of hypertension in this important ethnic group.

DESIGN NARRATIVE:

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).

The study was renewed in FY 2000. To further elucidate the environmental pathways, the investigators conducted a substudy cross-classifying participants on the major risk determinants (ie, obesity and sodium intake) and they examined gene-environment interactions directly. They used a genome scan in linkage analysis to identify new chromosomal regions of interest. They also examine two new candidate loci (adducin and beta-2 adrenergic receptor) and conducted association studies using single nucleotide polymorphisms. They used the full range of analytic tools, including segregation, linkage and cladistic analysis.

The study was renewed again in FY 2005 to : supplement evidence of hypertension causation on chromosomes 6,7, and 11 with a new set of dense markers and to search for positional candidate genes for hypertension at the two best regions; identify the genes under the linkage peak(s), find appropriate single nucleotide polymorphisms for a frequency of greater than 10% and conduct association/linkage disequilibrium mapping; replicate these findings in additional case-control studies and assess potential gene-environment interactions.

Study Type

Observational

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

No older than 100 years (ADULT, OLDER_ADULT, CHILD)

Accepts Healthy Volunteers

No

Genders Eligible for Study

All

Description

No eligibility criteria

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Collaborators and Investigators

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Sponsor

National Heart, Lung, and Blood Institute (NHLBI)

Investigators

  • Richard Cooper, Loyola University

Publications and helpful links

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General Publications

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start

September 1, 1995

Primary Completion (ACTUAL)

December 1, 2008

Study Completion (ACTUAL)

December 1, 2008

Study Registration Dates

First Submitted

May 25, 2000

First Submitted That Met QC Criteria

May 25, 2000

First Posted (ESTIMATE)

May 26, 2000

Study Record Updates

Last Update Posted (ESTIMATE)

July 12, 2016

Last Update Submitted That Met QC Criteria

July 11, 2016

Last Verified

December 1, 2008

More Information

Terms related to this study

Additional Relevant MeSH Terms

Other Study ID Numbers

  • 4293
  • R01HL053353 (NIH)

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

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