Racial Variation in ACE--Genetic and Physiologic Bases

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00005757
First received: May 25, 2000
Last updated: June 23, 2005
Last verified: March 2005
  Purpose

To determine whether differences in the activity of the renin-angiotensin and bradykinin systems are involved in the pathogenesis of blood pressure variation in African Americans.


Condition
Cardiovascular Diseases
Heart Diseases
Hypertension

Study Type: Observational

Resource links provided by NLM:


Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 1997
Estimated Study Completion Date: August 2001
Detailed Description:

BACKGROUND:

Each year, more than 40,000 new patients require treatment for end stage renal disease, a condition which is 4-fold higher among African Americans than Caucasians. Trials of angiotensin converting enzyme inhibitors (ACEIs) in Caucasians support a role of the renin-angiotensin system in the pathogenesis of glomerulosclerosis. Yet, despite the high prevalence of nephropathy among African Americans, Blacks have been under-represented in studies in ACEIs. Data from our laboratory suggest that the renal effects of ACEI may differ in African Americans. African Americans are resistant to the anti-hypertensive effects of ACEI and, thus, may be resistant to the renoprotective effects as well. The ACE deletion allele, a variant associated with increased ACE activity and progression of renal diseases, is increased in frequency in African Americans, while the frequency of the Ang AT1 receptor C allele, a variant associated with antihypertensive responsiveness to ACEI is decreased. Moreover, African Americans exhibit decreased sensitivity to Ang I and increased sensitivity to bradykinin. Taken together, these data suggest the hypothesis that ACE activity is increased in African Americans, leading to decreased bradykinin levels ( and receptor sensitization) and increased tissue Ang II (and receptor desensitization).

DESIGN NARRATIVE:

The study tests the hypothesis that ACE activity is increased in African Americans, leading to decreased bradykinin levels (and receptor sensitization) and increased tissue Ang II (and receptor desensitization). The effects of race, hypertension and ACE insertion/deletion genotype on ACE activity will be determined, as measured by the pressor and renal vasoconstrictor responses to Ang I and Ang II and the vasodilator response to bradykinin. Specific bradykinin and angiotensin receptor antagonists will be used to determine the relative contribution of increased bradykinin and decreased angiotensin II to the renal hemodynamic effects of ACEIs in African Americans and Caucasians.

  Eligibility

Genders Eligible for Study:   Male
Accepts Healthy Volunteers:   No
Criteria

No eligibility criteria

  Contacts and Locations
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Please refer to this study by its ClinicalTrials.gov identifier: NCT00005757

Sponsors and Collaborators
Investigators
Investigator: Nancy Brown Vanderbilt University
  More Information

Publications:

ClinicalTrials.gov Identifier: NCT00005757     History of Changes
Other Study ID Numbers: 5115
Study First Received: May 25, 2000
Last Updated: June 23, 2005
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases
Hypertension
Vascular Diseases

ClinicalTrials.gov processed this record on September 22, 2014