This application is based on the hypothesis that changes in salt intake lead to changes in circulating levels of the hormone, angiotensin II (AII). Subsequent alterations in AII levels act via the brainstein site known as the area postrema to create neurogenic changes in medullary sympathetic activity. More specifically, an increase in salt intake will decrease circulating levels of AII via suppression of the renin-angiotensin system (RAS). Decreased concentrations of AII at the area postrema will cause a withdrawal of sympathetic tone to the kidneys and vasculature. Suppression of the RAS along with withdrawal of sympathetic tone allows for the preservation of arterial pressure, as well as sodium and volume homeostasis. It is hypothesized that any intervention in this NaCl-AII- Sympathetic Reflex (during increases in NaCl intake) will result in a lack of salt induced sympathoinhibition and salt induced hypertension. Dr. John Collister received his D.V.M. in 1994 from the Univ. of IL. He is now currently working toward a Ph.D. in the Dept. of Vet. PathoBiology at the Univ. of MN. The applicant has both a strong academic and research background. He has chosen a research career in the biomedical sciences of integrated cardiovascular physiology. During the initial two years of support from this award, Dr. Collister will be under the direct supervision of the sponsor, Dr. John Osborn. During this time, 100% effort will be placed on the proposed research while the candidate completes his Ph.D. thesis. Dr. Osborn has trained successful scientists in the past and is a well known and respected scientist both locally and nationally, in the field of hypertension research. Upon completion of his Ph.D., Dr. Collister will be appointed to an Assistant Professorship within the Dept. of Vet. PathoBiology. At this time, 80% effort will be placed on the proposed research, while other time will be utilized teaching classes within the College of Veterinary Medicine (Anatomy and Physiology). In addition, the advisory committee will meet regularly to discuss research data and future directions. This committee is made up of diverse individuals who are all active and trained researchers in specific areas of the RAS. Dr. Collister will also have the opportunity to interact with individuals from the Departments of Pharmacology, Neuroscience, and Cellular and Integrative Physiology, through attending regular journal clubs and seminars. Upon completion, Dr. Collister will have fully developed into an independent investigator.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08HL003790-02
Application #
6030414
Study Section
Special Emphasis Panel (ZHL1-CSR-Y (M2))
Project Start
1998-07-01
Project End
2003-06-30
Budget Start
1999-09-17
Budget End
2000-06-30
Support Year
2
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Minnesota Twin Cities
Department
Type
Schools of Arts and Sciences
DUNS #
168559177
City
Minneapolis
State
MN
Country
United States
Zip Code
55455
Collister, John P; Hendel, Michael D (2005) Chronic effects of angiotensin II and at1 receptor antagonists in subfornical organ-lesioned rats. Clin Exp Pharmacol Physiol 32:462-6
Collister, John P; Osborn, John W (2005) Role of a responsive sympathetic nervous system in the chronic hypotensive effects of losartan in normal rats. J Cardiovasc Pharmacol 46:147-54
Collister, John P; Hendel, Michael D (2003) The role of Ang (1-7) in mediating the chronic hypotensive effects of losartan in normal rats. J Renin Angiotensin Aldosterone Syst 4:176-9
Collister, John P; Hendel, Michael D (2003) Role of the subfornical organ in the chronic hypotensive response to losartan in normal rats. Hypertension 41:576-82
Collister, John P; Soucheray, Sandra L; Osborn, John W (2002) Chronic hypotensive effects of losartan are not dependent on the actions of angiotensin II at AT 2 receptors. J Cardiovasc Pharmacol 39:107-16
Collister, J P; Osborn, J W (1999) The chronic infusion of hexamethonium and phenylephrine to effectively clamp sympathetic vasomotor tone. A novel approach. J Pharmacol Toxicol Methods 42:135-47