The finding of CRH-R2 in cardiac tissue leads to the hypothesis tested in this proposal: cardiac-specific responses to CRH occur via CRH receptors localized in the heart. The primary prediction is that certain specific cardiac effects of CRH occur through CRH-R2. The source of CRH that acts on the cardiac CRH-R2 may be via local synthesis in the heart and /or from production in the central nervous system.
The aims are:
Aim 1 : Determine which cells in the mouse heart express CRH receptors.
Aim 2 : To examine the interaction of two peptide ligands, CRH and urocortin, with the CRH-R2 receptor and to determine the second messenger systems to which the receptor is coupled.
Aim 3 : Determine the mechanism(s) involved in cardiac CRH-R2 regulation by the stress-related stimulus, bacterial endotoxin.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
1R29HL055512-01A2
Application #
2029673
Study Section
Endocrinology Study Section (END)
Project Start
1997-06-01
Project End
2002-04-30
Budget Start
1997-06-01
Budget End
1998-04-30
Support Year
1
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Oregon Health and Science University
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
009584210
City
Portland
State
OR
Country
United States
Zip Code
97239