Cardiovascular DiseasesNCT00005268
Family Blood Pressure Program - GenNet Network
An observational study of Cardiovascular Diseases and Heart Diseases, run by National Heart, Lung, and Blood Institute (NHLBI).
Trial summary
To identify new genetic loci regulating blood pressure in hypertensive rats and in case-controls from relevant human populations. The study consists of a four grant network, which in turn is part of an NHLBI initiative, the Family Blood Pressure Program (FBPP) consisting of four networks. Read more about this study
- Who is it for?
- Ages Up to 100 years, men only
- Conditions the study is for
- Cardiovascular Diseases, Heart Diseases, Hypertension
- How many people
- Not given
- Where
- No sites listed yet
- Study dates
- Sep 1995to Aug 2008
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Up to 100 years
- Men only
- No healthy volunteers
- Child, Adult, Older adult
No eligibility criteria
About this study
To identify new genetic loci regulating blood pressure in hypertensive rats and in case-controls from relevant human populations. The study consists of a four grant network, which in turn is part of an NHLBI initiative, the Family Blood Pressure Program (FBPP) consisting of four networks.
Read the detailed description
BACKGROUND:
Hypertension, a complex disease involving the interplay of genetic and environmental factors, affects an estimated 50 million Americans and is a major predisposing factor for myocardial infarction, vascular disease, stroke, and renal failure. It has been estimated from segregation analysis and twin studies that approximately 45 percent of the interindividual differences in blood pressure are accounted for by genetic differences. The identification of the genes whose variants contribute to high blood pressure will have far-reaching effects on our understanding of the pathophysiology of the circulation and may suggest new preventive measures and rational therapeutic approaches.
One of the principal advantages of the genetic approach is that it identifies primary molecular defects. As a result, it will be possible to stratify the general hypertensive population into subgroups based on genotype and intermediate phenotype and thereby evaluate preventive strategies and therapeutic approaches in more homogeneous groups. In addition, the identification of hypertensive genes also provides the basis for an understanding of the interactions between genes and environmental factors. It is very likely that particular environmental variables exert their effects only in the presence of certain genotypes.
Until recently, the techniques for dissecting the genetic determinants of high blood pressure were not available or were not developed to an extent that would make the Family Blood Pressure Program initiative feasible. However, several recent advances in technology and analytical methods, together with the rapid construction of genetic maps, have substantially improved the chances of detecting these genetic factors.
The concept for the Family Blood Pressure Program was conceived in the Report of the Expert Panel on Genetic Strategies for Heart, Lung, and Blood Diseases. The initiative was approved by the Arteriosclerosis, Hypertension, and Lipid Metabolism Advisory Committee (AHLMAC) in March, 1993. The genetic-epidemiological aspects were approved by the Clinical Applications and Prevention Advisory Committee (CAPAC) in February, 1993. The Request for Applications was released in March, 1994. Awards were made in September, 1995.
DESIGN NARRATIVE:
The network consists of five centers: two field centers, a rat genotyping center, a human genotyping center with statistical genetics and informatics, and a genetic analysis center. After genetic loci regulating blood pressure are identified, genomic markers are used to study genetic linkage with red blood cell lithium-sodium countertransport, hyperkinetic hyperadrenergic state, and the renin-angiotensin system in sibships and tested in several Black populations.
The well-characterized Tecumseh population was utilized as a first step in determining genetic linkage to hypertension, using the quantitative trait locus (QTL) approach. A total of 250 white sibships in the Tecumseh population were examined using 400 anonymous markers and candidate genes. Approximately 100 markers that demonstrated linkage were used to examine 250 African-American sibships in Maywood, Illinois. Fifty refined candidate markers were used to study several extant Black populations in Jamaica and Nigeria, as well as individuals in the other two populations. A unique feature of the network is the inclusion of a rat genotyping center. Crosses of inbred hypertensive and normotensive rats are used to identify genomic regions linked to hypertension. The regions are then used to identify homologous human candidate genes in addition to those already selected from previous research.
The GenNet Network was renewed in September 2000 to continue studies of hypertension-associated phenotypes in United States whites, African Americans, Mexican Americans, and West Africans and Caribbeans. The Family Blood Pressure Program as a whole carried out five specific aims in the renewal period. These aims were grouped according to two complementary themes: First, the investigators created and analyzed a database of blood pressure-related phenotype and genotype data from all FBPP participants (Aim 1). Within linked regions, they identified allelic variation within positional candidate genes and evaluated the relationship of these polymorphisms with blood pressure levels and hypertension status (Aims 2 and 3). Second, they used quantitative measures of target organ damage to identify genes that influenced susceptibility to develop hypertensive heart and kidney diseases (Aims 4 and 5). In addition to the Program specific aims, each network, including GenNet, carried out its own specific aims alone, based on unique aspects of their population and interests and expertise of the investigators. In GenNet, progress has been made in the identification of single nucleotide polymorphisms (SNPs) in candidate genes and work was underway to develop rapid genotyping methods in individual and pool samples. The search for genes in diverse human populations was complemented by mapping studies in rat strains, in which linked regions that overlap with regions showing evidence for linkage in the human studies were selected for positional cloning.
In the next phase of the FBPP ending in August, 2008, a major emphasis is placed on making the Program a shared resource for hypertension researchers in the United States and throughout the world. In Aim 1, the investigators will build, maintain and update a publicly available knowledge-base to facilitate research by non-FBPP investigators on the genetics of hypertension, its risk factors and its complications. In Aim 2, they will use state-of-the-art genetic linkage analysis methods to identify additional linkage regions using subgroups of pedigrees and physiologically relevant combinations of phenotypes that will aid in localizing hypertension genes. In Aim 3, they will use a combination of bioinformatics, a dense array of SNPs, and state-of-the-art data analysis to follow-up regions of interest and identify the underlying hypertension genes. The regions to be followed-up include those identified during the current phase of the FBPP and Aim 2 of this renewal phase. In Aim 4, they will evaluate the hypertension genes identified in Aim 3 for their association with multiple measures reflecting the cardiovascular and renal complications of hypertension, including left ventricular mass and microalbuminuria. It is the long-term goal of the FBPP to have the hypertension genetics community develop a comprehensive picture of the genetic architecture of human hypertension, including its risk factors, complications, and response to treatment.
- Conditions
- Cardiovascular Diseases, Heart Diseases, Hypertension
- Medical subject headings
- Cardiovascular Diseases, Heart Diseases, Hypertension
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 May 2000 (estimated)
- Study startSep 1995
- Primary completionAug 2008
- Study completionAug 2008
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (30)Papers the sponsor has linked to this study.
- Other trials for Cardiovascular DiseasesStudies of the same condition, open and under way.
- More trials run by National Heart, Lung, and Blood Institute (NHLBI)The sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
Sponsor and investigators
- Sponsor type
- US National Institutes of Health
- Investigators
- Aravinda Chakravarti, Case Western Reserve UniversityRichard Cooper, Loyola UniversityHoward Jacob, Medical College of WisconsinNicholas Schork, Case Western Reserve UniversityAlan Weder, University of Michigan
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00005268
- Sponsor's protocol ID
- 1152
- Other IDs
- 5U01HL054512
- Status last verified
- Aug 2008
- First submitted
- 25 May 2000
- Last updated
- 8 Aug 2016
- Results posted
- No
Publications
Koike G, Miano JM, Vanvooren P, Shiozawa M, Szpirer C, Jacob HJ. Mapping of the rat SM22 gene to chromosome 8q24: a candidate for high blood pressure and cardiac hypertrophy. Mamm Genome. 1998 Jan;9(1):76-7. doi: 10.1007/s003359900684. No abstract available.
PubMed 9434951Innes BA, McLaughlin MG, Kapuscinski MK, Jacob HJ, Harrap SB. Independent genetic susceptibility to cardiac hypertrophy in inherited hypertension. Hypertension. 1998 Mar;31(3):741-6. doi: 10.1161/01.hyp.31.3.741.
PubMed 9495256Young EA, Nesse RM, Weder A, Julius S. Anxiety and cardiovascular reactivity in the Tecumseh population. J Hypertens. 1998 Dec;16(12 Pt 1):1727-33. doi: 10.1097/00004872-199816120-00004.
PubMed 9869005Halushka MK, Fan JB, Bentley K, Hsie L, Shen N, Weder A, Cooper R, Lipshutz R, Chakravarti A. Patterns of single-nucleotide polymorphisms in candidate genes for blood-pressure homeostasis. Nat Genet. 1999 Jul;22(3):239-47. doi: 10.1038/10297.
PubMed 10391210Province MA, Boerwinkle E, Chakravarti A, Cooper R, Fornage M, Leppert M, Risch N, Ranade K. Lack of association of the angiotensinogen-6 polymorphism with blood pressure levels in the comprehensive NHLBI Family Blood Pressure Program. National Heart, Lung and Blood Institute. J Hypertens. 2000 Jul;18(7):867-76. doi: 10.1097/00004872-200018070-00008.
PubMed 10930184Stoll M, Kwitek-Black AE, Cowley AW Jr, Harris EL, Harrap SB, Krieger JE, Printz MP, Provoost AP, Sassard J, Jacob HJ. New target regions for human hypertension via comparative genomics. Genome Res. 2000 Apr;10(4):473-82. doi: 10.1101/gr.10.4.473.
PubMed 10779487Fan JB, Chen X, Halushka MK, Berno A, Huang X, Ryder T, Lipshutz RJ, Lockhart DJ, Chakravarti A. Parallel genotyping of human SNPs using generic high-density oligonucleotide tag arrays. Genome Res. 2000 Jun;10(6):853-60. doi: 10.1101/gr.10.6.853.
PubMed 10854416Cowley AW Jr, Roman RJ, Kaldunski ML, Dumas P, Dickhout JG, Greene AS, Jacob HJ. Brown Norway chromosome 13 confers protection from high salt to consomic Dahl S rat. Hypertension. 2001 Feb;37(2 Pt 2):456-61. doi: 10.1161/01.hyp.37.2.456.
PubMed 11230318Zhu X, Cooper RS, Luke A, Chen G, Wu X, Kan D, Chakravarti A, Weder A. A genome-wide scan for obesity in African-Americans. Diabetes. 2002 Feb;51(2):541-4. doi: 10.2337/diabetes.51.2.541.
PubMed 11812767Wu X, Cooper RS, Borecki I, Hanis C, Bray M, Lewis CE, Zhu X, Kan D, Luke A, Curb D. A combined analysis of genomewide linkage scans for body mass index from the National Heart, Lung, and Blood Institute Family Blood Pressure Program. Am J Hum Genet. 2002 May;70(5):1247-56. doi: 10.1086/340362. Epub 2002 Mar 28.
PubMed 11923912Glidden DV, Liang KY. Ascertainment adjustment in complex diseases. Genet Epidemiol. 2002 Oct;23(3):201-8. doi: 10.1002/gepi.10204.
PubMed 12384971Lalouel JM. Large-scale search for genes predisposing to essential hypertension. Am J Hypertens. 2003 Feb;16(2):163-6. doi: 10.1016/s0895-7061(02)03201-6. No abstract available.
PubMed 12559687Shaw SH, Carrasquillo MM, Kashuk C, Puffenberger EG, Chakravarti A. Allele frequency distributions in pooled DNA samples: applications to mapping complex disease genes. Genome Res. 1998 Feb;8(2):111-23. doi: 10.1101/gr.8.2.111.
PubMed 9477339Wu X, Cooper RS, Boerwinkle E, Turner ST, Hunt S, Myers R, Olshen RA, Curb D, Zhu X, Kan D, Luke A. Combined analysis of genomewide scans for adult height: results from the NHLBI Family Blood Pressure Program. Eur J Hum Genet. 2003 Mar;11(3):271-4. doi: 10.1038/sj.ejhg.5200952.
PubMed 12673281Thiel BA, Chakravarti A, Cooper RS, Luke A, Lewis S, Lynn A, Tiwari H, Schork NJ, Weder AB. A genome-wide linkage analysis investigating the determinants of blood pressure in whites and African Americans. Am J Hypertens. 2003 Feb;16(2):151-3. doi: 10.1016/s0895-7061(02)03246-6.
PubMed 12559684
Study at a glance
From the registry record, last updated by the sponsor on 8 Aug 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Family Blood Pressure Program - GenNet Network
- ClinicalTrials.gov ID
- NCT00005268
- Acronym / sponsor ID
- 1152
- Conditions
- Cardiovascular Diseases, Heart Diseases, Hypertension
- Study type
- Observational
- Recruitment status
- Completed
- Lead sponsor
- National Heart, Lung, and Blood Institute (NHLBI)US National Institutes of Health
- Study start
- Sep 1995
- Primary completion
- Aug 2008 (actual)
- Study completion
- Aug 2008 (actual)
- First posted
- 26 May 2000 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
To identify new genetic loci regulating blood pressure in hypertensive rats and in case-controls from relevant human populations. The study consists of a four grant network, which in turn is part of an NHLBI initiative, the Family Blood Pressure Program (FBPP) consisting of four networks.
Detailed description
BACKGROUND:
Hypertension, a complex disease involving the interplay of genetic and environmental factors, affects an estimated 50 million Americans and is a major predisposing factor for myocardial infarction, vascular disease, stroke, and renal failure. It has been estimated from segregation analysis and twin studies that approximately 45 percent of the interindividual differences in blood pressure are accounted for by genetic differences. The identification of the genes whose variants contribute to high blood pressure will have far-reaching effects on our understanding of the pathophysiology of the circulation and may suggest new preventive measures and rational therapeutic approaches.
One of the principal advantages of the genetic approach is that it identifies primary molecular defects. As a result, it will be possible to stratify the general hypertensive population into subgroups based on genotype and intermediate phenotype and thereby evaluate preventive strategies and therapeutic approaches in more homogeneous groups. In addition, the identification of hypertensive genes also provides the basis for an understanding of the interactions between genes and environmental factors. It is very likely that particular environmental variables exert their effects only in the presence of certain genotypes.
Until recently, the techniques for dissecting the genetic determinants of high blood pressure were not available or were not developed to an extent that would make the Family Blood Pressure Program initiative feasible. However, several recent advances in technology and analytical methods, together with the rapid construction of genetic maps, have substantially improved the chances of detecting these genetic factors.
The concept for the Family Blood Pressure Program was conceived in the Report of the Expert Panel on Genetic Strategies for Heart, Lung, and Blood Diseases. The initiative was approved by the Arteriosclerosis, Hypertension, and Lipid Metabolism Advisory Committee (AHLMAC) in March, 1993. The genetic-epidemiological aspects were approved by the Clinical Applications and Prevention Advisory Committee (CAPAC) in February, 1993. The Request for Applications was released in March, 1994. Awards were made in September, 1995.
DESIGN NARRATIVE:
The network consists of five centers: two field centers, a rat genotyping center, a human genotyping center with statistical genetics and informatics, and a genetic analysis center. After genetic loci regulating blood pressure are identified, genomic markers are used to study genetic linkage with red blood cell lithium-sodium countertransport, hyperkinetic hyperadrenergic state, and the renin-angiotensin system in sibships and tested in several Black populations.
The well-characterized Tecumseh population was utilized as a first step in determining genetic linkage to hypertension, using the quantitative trait locus (QTL) approach. A total of 250 white sibships in the Tecumseh population were examined using 400 anonymous markers and candidate genes. Approximately 100 markers that demonstrated linkage were used to examine 250 African-American sibships in Maywood, Illinois. Fifty refined candidate markers were used to study several extant Black populations in Jamaica and Nigeria, as well as individuals in the other two populations. A unique feature of the network is the inclusion of a rat genotyping center. Crosses of inbred hypertensive and normotensive rats are used to identify genomic regions linked to hypertension. The regions are then used to identify homologous human candidate genes in addition to those already selected from previous research.
The GenNet Network was renewed in September 2000 to continue studies of hypertension-associated phenotypes in United States whites, African Americans, Mexican Americans, and West Africans and Caribbeans. The Family Blood Pressure Program as a whole carried out five specific aims in the renewal period. These aims were grouped according to two complementary themes: First, the investigators created and analyzed a database of blood pressure-related phenotype and genotype data from all FBPP participants (Aim 1). Within linked regions, they identified allelic variation within positional candidate genes and evaluated the relationship of these polymorphisms with blood pressure levels and hypertension status (Aims 2 and 3). Second, they used quantitative measures of target organ damage to identify genes that influenced susceptibility to develop hypertensive heart and kidney diseases (Aims 4 and 5). In addition to the Program specific aims, each network, including GenNet, carried out its own specific aims alone, based on unique aspects of their population and interests and expertise of the investigators. In GenNet, progress has been made in the identification of single nucleotide polymorphisms (SNPs) in candidate genes and work was underway to develop rapid genotyping methods in individual and pool samples. The search for genes in diverse human populations was complemented by mapping studies in rat strains, in which linked regions that overlap with regions showing evidence for linkage in the human studies were selected for positional cloning.
In the next phase of the FBPP ending in August, 2008, a major emphasis is placed on making the Program a shared resource for hypertension researchers in the United States and throughout the world. In Aim 1, the investigators will build, maintain and update a publicly available knowledge-base to facilitate research by non-FBPP investigators on the genetics of hypertension, its risk factors and its complications. In Aim 2, they will use state-of-the-art genetic linkage analysis methods to identify additional linkage regions using subgroups of pedigrees and physiologically relevant combinations of phenotypes that will aid in localizing hypertension genes. In Aim 3, they will use a combination of bioinformatics, a dense array of SNPs, and state-of-the-art data analysis to follow-up regions of interest and identify the underlying hypertension genes. The regions to be followed-up include those identified during the current phase of the FBPP and Aim 2 of this renewal phase. In Aim 4, they will evaluate the hypertension genes identified in Aim 3 for their association with multiple measures reflecting the cardiovascular and renal complications of hypertension, including left ventricular mass and microalbuminuria. It is the long-term goal of the FBPP to have the hypertension genetics community develop a comprehensive picture of the genetic architecture of human hypertension, including its risk factors, complications, and response to treatment.
Study design
Who may qualify
- Ages
- Up to 100 years
- Sex
- Male only
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 8 Aug 2016.
- Background: PubMed 9434951Koike G, Miano JM, Vanvooren P, Shiozawa M, Szpirer C, Jacob HJ. Mapping of the rat SM22 gene to chromosome 8q24: a candidate for high blood pressure and cardiac hypertrophy. Mamm Genome. 1998 Jan;9(1):76-7. doi: 10.1007/s003359900684. No abstract available.
- Background: PubMed 9495256Innes BA, McLaughlin MG, Kapuscinski MK, Jacob HJ, Harrap SB. Independent genetic susceptibility to cardiac hypertrophy in inherited hypertension. Hypertension. 1998 Mar;31(3):741-6. doi: 10.1161/01.hyp.31.3.741.
- Background: PubMed 9869005Young EA, Nesse RM, Weder A, Julius S. Anxiety and cardiovascular reactivity in the Tecumseh population. J Hypertens. 1998 Dec;16(12 Pt 1):1727-33. doi: 10.1097/00004872-199816120-00004.
- Background: PubMed 10391210Halushka MK, Fan JB, Bentley K, Hsie L, Shen N, Weder A, Cooper R, Lipshutz R, Chakravarti A. Patterns of single-nucleotide polymorphisms in candidate genes for blood-pressure homeostasis. Nat Genet. 1999 Jul;22(3):239-47. doi: 10.1038/10297.
- Background: PubMed 10930184Province MA, Boerwinkle E, Chakravarti A, Cooper R, Fornage M, Leppert M, Risch N, Ranade K. Lack of association of the angiotensinogen-6 polymorphism with blood pressure levels in the comprehensive NHLBI Family Blood Pressure Program. National Heart, Lung and Blood Institute. J Hypertens. 2000 Jul;18(7):867-76. doi: 10.1097/00004872-200018070-00008.
- Background: PubMed 10779487Stoll M, Kwitek-Black AE, Cowley AW Jr, Harris EL, Harrap SB, Krieger JE, Printz MP, Provoost AP, Sassard J, Jacob HJ. New target regions for human hypertension via comparative genomics. Genome Res. 2000 Apr;10(4):473-82. doi: 10.1101/gr.10.4.473.
- Background: PubMed 10854416Fan JB, Chen X, Halushka MK, Berno A, Huang X, Ryder T, Lipshutz RJ, Lockhart DJ, Chakravarti A. Parallel genotyping of human SNPs using generic high-density oligonucleotide tag arrays. Genome Res. 2000 Jun;10(6):853-60. doi: 10.1101/gr.10.6.853.
- Background: PubMed 11230318Cowley AW Jr, Roman RJ, Kaldunski ML, Dumas P, Dickhout JG, Greene AS, Jacob HJ. Brown Norway chromosome 13 confers protection from high salt to consomic Dahl S rat. Hypertension. 2001 Feb;37(2 Pt 2):456-61. doi: 10.1161/01.hyp.37.2.456.
- Background: PubMed 11812767Zhu X, Cooper RS, Luke A, Chen G, Wu X, Kan D, Chakravarti A, Weder A. A genome-wide scan for obesity in African-Americans. Diabetes. 2002 Feb;51(2):541-4. doi: 10.2337/diabetes.51.2.541.
- Background: PubMed 11923912Wu X, Cooper RS, Borecki I, Hanis C, Bray M, Lewis CE, Zhu X, Kan D, Luke A, Curb D. A combined analysis of genomewide linkage scans for body mass index from the National Heart, Lung, and Blood Institute Family Blood Pressure Program. Am J Hum Genet. 2002 May;70(5):1247-56. doi: 10.1086/340362. Epub 2002 Mar 28.
- Background: PubMed 12384971Glidden DV, Liang KY. Ascertainment adjustment in complex diseases. Genet Epidemiol. 2002 Oct;23(3):201-8. doi: 10.1002/gepi.10204.
- Background: PubMed 12559687Lalouel JM. Large-scale search for genes predisposing to essential hypertension. Am J Hypertens. 2003 Feb;16(2):163-6. doi: 10.1016/s0895-7061(02)03201-6. No abstract available.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Aravinda Chakravarti
Case Western Reserve University
Richard Cooper
Loyola University
Howard Jacob
Medical College of Wisconsin
Questions about this trial
What is this clinical trial studying?
An observational study of Cardiovascular Diseases and Heart Diseases, run by National Heart, Lung, and Blood Institute (NHLBI).
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 8 Aug 2016. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00005268, which also lists 30 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 8 Aug 2016.