Abstract

The hypothesis of this project is that an increase in uterine artery vasodilator production is associated with a marked increase in AT1-R expression and/or coupling of existing AT1-R in uterine artery endothelial cells.
Aim 1 is to investigate, using 5-RACE cloning + RT/PCR assays, if there are pregnancy-specific isoforms of AT1-R mRNA in uterine artery endothelial cells.
Aim 2 is to establish in vivo that pregnancy-induced changes in AT1-R expression are due to direct or indirect, via bFGF or VEGF, actions of estrogen.
Aim 3 is to determine in vitro whether changes in expression result from changes in phospholipase C and PGI2 production.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29HL056702-02
Application #
2735326
Study Section
Human Embryology and Development Subcommittee 1 (HED)
Project Start
1997-08-15
Project End
2002-06-30
Budget Start
1998-07-01
Budget End
1999-06-30
Support Year
2
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
University of Wisconsin Madison
Department
Obstetrics & Gynecology
Type
Schools of Medicine
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715