Evaluating the Relationship Between Inflammation, Genetics, and Stress in the Development of High Blood Pressure

NCT ID: NCT00384241

Last Updated: 2015-06-03

Study Results

Results available

Outcome measurements, participant flow, baseline characteristics, and adverse events have been published for this study.

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Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

1099 participants

Study Classification

OBSERVATIONAL

Study Start Date

2006-08-31

Study Completion Date

2009-07-31

Brief Summary

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High blood pressure affects nearly one third of all individuals in the United States. If left untreated, it can lead to stroke, heart failure, heart attack, kidney failure, or blindness. For many people, the exact cause of high blood pressure is unknown, but it is believed that both genetic and environmental factors contribute to the development of the condition. The purpose of this study is to examine the importance of genetics, inflammation, and stress on the development of high blood pressure.

Detailed Description

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High blood pressure is a complex condition that can be caused by many factors, including obesity, diet, genetics, or stress. Maintaining a healthy balance of sodium in the body is important for adequate blood pressure control. Some individuals experience sustained high blood pressure during periods of extended stress, combined with the inability to excrete enough sodium through urine to re-establish normal blood pressure levels. This type of stress-induced high blood pressure is related to interleukin-6 (IL-6), a protein that stimulates inflammation and immune responses. To determine the interaction between stress, inflammation, and genetics, this study will examine the role of IL-6 in regulating sodium levels and blood pressure in individuals undergoing stress. This information will be useful in determining new ways to evaluate risk factors for high blood pressure.

This study will examine previously collected DNA samples from young adults who participated in prior genetic studies. There will be no study visits for participants. IL-6, IL-6R, glycoprotein 130 (gp130), and C-reactive protein (CRP) genes will be analyzed in all samples; changes in plasma levels of IL-6 and CRP in response to stress will be examined in selected samples. The parents of participants will be asked to provide cheek swabs for additional DNA analysis.

Conditions

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Hypertension

Study Design

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Observational Model Type

COHORT

Study Time Perspective

RETROSPECTIVE

Study Groups

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Children

Children age 15-19, self reported as African American of European Origin, healthy non-smoker, with normal blood pressure, exposed to an activity to that results in induced stress

Induced Stress

Intervention Type BEHAVIORAL

Participation in an active coping task by playing a video game against another participant.

Parents

Collection of buccal swab Parent of participants in the Children Arm

Buccal Swab

Intervention Type PROCEDURE

One Buccal swab collected from each parent

Interventions

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Induced Stress

Participation in an active coping task by playing a video game against another participant.

Intervention Type BEHAVIORAL

Buccal Swab

One Buccal swab collected from each parent

Intervention Type PROCEDURE

Eligibility Criteria

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Inclusion Criteria

* Participated in two previous NIH funded studies HL073260, HL077230
* Biological parents willing to participate in the study
* African American or European origins

Exclusion Criteria

* Non-biological parents
Minimum Eligible Age

15 Years

Maximum Eligible Age

19 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role collaborator

Augusta University

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Haidong Zhu, MD, PhD

Role: PRINCIPAL_INVESTIGATOR

Augusta University

Locations

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Medical College of Georgia, Georgia Regents University

Augusta, Georgia, United States

Site Status

Countries

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United States

Other Identifiers

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R21HL085817

Identifier Type: NIH

Identifier Source: secondary_id

View Link

1R21HL085817-01

Identifier Type: NIH

Identifier Source: secondary_id

View Link

1359

Identifier Type: -

Identifier Source: org_study_id

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