Pharmacology & Toxicology Faculty
Dr. Northcott PhotoCarrie A. Northcott, Assistant Professor
1993 AS, Black Hawk College
1995 BS, Agronomy, University of Illinois
1998 MS, Crop Sciences, University of Illinois
2003 PhD, Pharmacology and Toxicology, Michigan State University
2003-2008 Postdoctoral Research, Dept. of Pharmacology and Toxicology, Michigan State University
2008-present Assistant Professor, Department of Pharmacology and Toxicology, Michigan State University

   Contact Info:Email: taetscar@msu.edu Phone: 517-353-5326 Lab: B429 Life Sciences Bldg.
Research Summary

Click to review audio slideshow.

My laboratory is interested in examining the intracellular signaling pathways involved in the regulation of blood pressure, specifically in a region of the brain called the paraventricular nucleus (PVN). The PVN is known to be an integrative area of the brain hypothalamic region involved in the regulation of metabolic processes, stress responses, cardiovascular function/blood pressure regulation and the autonomic nervous system. The overall hypothesis of the laboratory is that hypertension is associated with increased excitatory neurotransmission that is the result of changes within intracellular signaling mechanisms in the PVN. The two intracellular signaling pathways of specific interest are phosphatidylinositol 3-kinase (PI3-kinase) and mitogen activated protein kinase (MAPK). These are complex pathways that located not only in the PVN, but in many regions of the body and involved in many biological endpoints. If these pathways within the PVN are overexpressed they may further amplify excitatory nuerotransmission resulting ultimately in hypertension.

Our laboratory uses an integrative approach, utilizing biochemical, gene transfer and physiological studies to examine intracellular signaling changes within the PVN that increase excitatory sympathoadrenal function and in turn elevate blood pressure. In addition, due to the integrative nature of the PVN, these data will also provide a glimpse at the role of signaling in other pathophysiological conditions, such as obesity.

Have you ever sat down with a
huge puzzle and thought, “Wow, what
a cool challenge!” That is what
intracellular signaling is to me --
a huge puzzle and a cool challenge
that is waiting to be explored. The
interesting part of this “puzzle” that
we are studying is that in most instances
some of the pieces are missing and we
can even re-use pieces, thus adding an
extra layer of complexity.

Professional Activities

  • American Physiological Society (APS)
  • American Society for Pharmacology and Experimental Therapeutics (ASPET)
  • Society for Experimental Biology and Medicine (SEBM)
  • American Heart Association Council of High Blood Pressure
  • Michigan State University Neuroscience Program

Grants

2001-2003 American Heart Association Predoctoral Grant- Midwest Affiliate
“Phosphoinositide 3-kinase upregulation in hypertension; a cause for enhanced arterial contraction and tone?”

2005-2006 American Heart Association Postdoctoral Grant- Midwest Affiliate
“Potential interrelationship between ROS and NO in the paraventricular nucleus in renal wrap hypertension?”

2006-2009 Ruth L. Kirschstein National Research Service Award “ROS and NO interaction in the PVN during hypertension?”

2006-2011 K99/R00 NIH Pathway to Independence Award (Learn more)
Paraventricular nucleus signaling mechanisms in hypertension”

Selected Publications

Northcott CA, Watts SW and Hsueh W. Vasoactive growth factors and adhesion molecules. In: Izzo, J.L. Jr. and Black, H.R. eds. Hypertension Primer, 3rd Edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2003; pp. 66-69.

Northcott CA, Poy MN, Najjar SM and Watts SW. PI3-kinase mediates enhanced spontaneous and agonist-induced contraction in aorta of DOCA-salt hypertensive rats. Circulation Research. 2002; 91:360-369.

Northcott CA, Hayflick JS and Watts SW. PI3-kinase upregulation and involvement in spontaneous tone in arteries from DOCA-salt rats: Is p110delta the culprit? Hypertension. 2004; 43(4):885-890.

Northcott CA, Hayflick JS and Watts SW. Upregulated function of phosphoinositide-3-kinase (PI3K) in genetically hypertensive rats: A moderator of arterial hypercontractility. Clinical and Experimental Pharmacology and Physiology. 2005; 32:851-858.

Northcott, C.A., Craig, T., Hinojosa-Laborde, C., Patel, K.P. and Haywood, J.R. A decrease in nitric oxide synthase in the paraventricular nucleus during the onset of renal wrap hypertension. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2007, Submitted.

Selected Abstracts

Northcott, C.A., Craig, T., Hinojosa-Laborde, C. and Haywood, J.R.: Decreased nitric oxide and increased superoxide in the PVN during renal wrap hypertension. Inter-American Society of Hypertension Meetings. April, 2005.

Zhao, H., Northcott, C.A., Fink, G.D., Mohankumar, P., Mohankumar, S. and Haywood, J.R.: Hypertension in diet-induced obese rats: Neurohumoral mechanisms contributing to blood pressure. Experimental Biology Meetings, 2006.

Northcott, C.A., Cox, L.A., Glenn, J., Haywood, J.R., Fink, G.D., Hinojosa-Laborde, C., Shade, R.E. Gene Expression profiling to define genetic mechanisms of salt-sensitive hypertension. Experimental Biology Meetings, 2006.

Northcott, C.A. and Haywood, J.R.: A loss of balance: Nitric oxide (NO) and superoxide (O2-) in the paraventricular nucleus (PVN) during the onset and chronic renal wrap hypertension. Experimental Biology Meetings, 2006.

Northcott, C.A.,King, A.J., Fink, G.D. and Haywood, J.R. Elevated angiotensin II-induced superoxide levels in the paraventricular nucleus during hypertension. American Heart Association-Council of High Blood Pressure Meetings, Fall 2006.

Northcott, C.A., and Haywood, J.R.: Inhibition of superoxide in the paraventricular nucleus blunts angiotensin II-induced elevations in blood pressure. Experimental Biology, 2007.

Northcott, C.A., Watts, S.W., Chen, Y., Morris, M., Chen, A. and Haywood, J.R.: Adenoviral inhibition of AT1a receptors in the paraventricular nucleus inhibits acute increases in mean arterial blood pressure in the rat. American Heart Association-Council of High Blood Pressure Meetings, Fall 2007.