It has been know for many years that the renin-angiotensin system contributes importantly to some forms of hypertension. Some studies suggest that angiotensin II may be an important stimulus for generation of reactive oxygen species in blood vessels. Although hypertension is known to be associated with vascular dysfunction, little is known regrading cellular and molecular mechanisms that are associated with these changes. The studies outlined in this proposal will use two novel murine models of hypertension (systemic model, R+/A+ and renal-specific model, R+/KA+).
The Specific Aims that will be examined are l) to examine the hypothesis that vascular dysfunction is present in the systemic model and renal- specific model. It is anticipated that the level of dysfunction will be greater in the systemic model as compared to the renal- specific model even though arterial pressure is similar in the two strains. 2) To examine the hypothesis that superoxide levels are enhanced within the vascular wall in the two models of hypertension. It is anticipated that levels of superoxide, which can inactivate NO, will be greater in the systemic model.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32HL010237-01
Application #
6013025
Study Section
Pathology A Study Section (PTHA)
Project Start
2000-01-15
Project End
Budget Start
2000-01-15
Budget End
2001-01-14
Support Year
1
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Iowa
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
041294109
City
Iowa City
State
IA
Country
United States
Zip Code
52242