The goal of the planned research is to either confirm or refute the presence of separate phosphatidylinositol 3 (PI3) and mitogen-activated protein (MAP) kinase pathways in the nucleus tract solitarius (NTS) in various models of hypertension. The overall objective is to investigate the signaling mechanisms at this brain site potentially contributing to development and maintenance of sustained hypertension. Our ongoing studies are designed to provide initial information about the relationship between the apparent enhancement of the sympathetic nervous system in various forms of hypertension and the role of PI3 and MAP kinase signaling pathways in the maintenance of hypertension. Our initial goal is to demonstrate that PI3 and MAP kinase signaling pathways in the NTS of (mRen-2)27 transgenic rats are activated in response to Ang II binding to AT1 receptors. The rationale for the proposed research is that, once knowledge of the mechanisms that are responsible for the development of hypertension has been obtained, it may lead to new strategies that can be used to prevent and/or treat hypertension, thereby reducing the morbidity and mortality associated with high blood pressure. ? ? ?

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31HL085927-01
Application #
7149459
Study Section
Special Emphasis Panel (ZRG1-DIG-H (29))
Program Officer
Meadows, Tawanna
Project Start
2006-08-15
Project End
2008-08-14
Budget Start
2006-08-15
Budget End
2007-08-14
Support Year
1
Fiscal Year
2006
Total Cost
$41,910
Indirect Cost
Name
Wake Forest University Health Sciences
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
937727907
City
Winston-Salem
State
NC
Country
United States
Zip Code
27157
Logan, Exazevia M; Aileru, Azeez A; Shaltout, Hossam A et al. (2011) The functional role of PI3K in maintenance of blood pressure and baroreflex suppression in (mRen2)27 and mRen2.Lewis rat. J Cardiovasc Pharmacol 58:367-73