Department of Cellular and Integrative Physiology

Our research focuses on the role of the central brain mechanisms on neurohormonal adjustments in cardiovascular regulation in the setting of experimental chronic heart failure. We are interested in the role of substances such as angiotensin II, nitric oxide and reactive oxidant stress as important mediators of sympathetic excitation in the setting of chronic heart failure. Molecular, cellular and whole animal techniques are used to understand abnormal cardiovascular and neural regulation in heart failure. In addition, we are extremely interested in the role of exercise training in ameliorating some of the abnormalities we have found in the central nervous system of animals with heart failure.

These techniques are providing important new information about normal cardiovascular physiology and about the pathophysiology of heart failure and other cardiovascular diseases.

Students in this laboratory learn surgical preparation of chronically instrumented animals and techniques for measuring a variety of cardiovascular parameters in awake, chronically instrumented animals. Molecular biological techniques such as Western blots, real time RT PCR and histological techniques are routinely used.

Recent publications:

1. Mitra AK, Gao L, Zucker IH. Angiotensin II-induced upregulation of AT1-receptor expression: Sequential activation of NFkB and Elk-1 in neurons. Am. J. Physiol. Cell Physiology (In Press, 2010). PMID: 20554912 
2. Kar S, Gao L, Zucker IH. Exercise training normalizes ACE and ACE2 in the brain of rabbits with pacing induced heart failure. J. Appl. Physiol., 108:923-932, 2010. [PMID: 20093667] 
3. Gao L, Li Y-L, Schultz HD, Wang W-Z, Finch M, Smith LM, Zucker IH. Kv4.3 Expression as a Potential Mechanism of Sympatho-Excitation in Heart Failure.  Am. J. Physiol. Heart and Circulatory Physiology, 298:H945-H955, 2010. [PubMed ID: 2044444] 
4. Zucker IH, Schultz HD, Patel KP, Wang W, Gao L. Regulation of central angiotensin type 1 receptors and sympathetic outflow in heart failure. Am. J. Physiol. Heart and Circulatory Physiology, 297(5): H1557-1566. 2009 [PubMed ID: 19717736] 
5. Gao L, Wang W-Z, Wang W, Zucker IH. Imbalance of angiotensin receptor expression and function in the rvlm: potential mechanism for sympathetic overactivity in heart failure. Hypertension 52:1-7, 2008.  [PubMed ID: 18768398]