James G Dobson PhD
|Institution||University of Massachusetts Medical School|
|Department||Microbiology and Physiological Systems|
|Address||University of Massachusetts Medical School|
55 Lake Avenue North
Worcester MA 01655
|Institution||UMMS - School of Medicine|
1965, B.S., Central Connecticut State University
1967, M.A., Wesleyan University
1971, Ph.D., University of Virginia
2008 - 2010, Professor & Interim Chairman of Physiology
2011 - Professor Emeritus
Regulation of neurotransmitter signal transduction in the heart
The research in this laboratory is concerned with investigating transmembrane signaling and the mechanisms which regulate cardiac muscle force development and myocardial energy utilization. Emphasis is given to the importance of adenosinergic modulation of the regulatory mechanisms particularly upon beta-adrenoceptor stimulation. The importance of the phosphorylation-dephosphorylation of proteins involved in the regulatory processes is a keen area of interest. Of additional interest is the role of adenosine in endothelial cell proliferation, aging of the cardiovascular system and heart failure. Mainly, isolated perfused hearts, dispersed ventricular myocytes and cultured endothelial cells are used in these studies.
The main emphasis is that by using current biochemical and molecular approaches and techniques the physiological mechanisms regulating cardiac mechanical performance and metabolism can be elucidated in the normal heart. This will foster a better understanding of how these neuro-regulatory mechanisms are altered in the diseased and aging cells that comprise the cardiovasculary system.
Adenosine and the Catecholamine Responses in Heart
A scheme illustrating that any one of the following: catacholamine stimulation of the heart, myocardial ischemia and adult heart aging, increases the concentration of myocardial adenosine. The increased adenosine in turn reduces the Beta-adrenergic induced increases in the myocardial chronotropic, inotropic and glycogenolytic responses of the heart and enhances coronary blood flow.
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