Medical Science Building (MSB) 185 South Orange Avenue Room H-655 Newark, NJ 07101 Phone: (973) 972-2863 Fax: (973) 972-7950
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Education
PHD, 2004, Howard University, Washington DC BS, 1993, South Carolina State University, Orangeburg SC 29117
Relevant Publications
DJ. Rozanski, DC. Renard-Rooney, Blackwell KN, M Solem and AP. Thomas (2010). Chronic ethanol consumption depresses beta-adrenergic responsiveness without changing basal excitation-contraction coupling in single rat cardiomyocytes. ( In preparation 2010).
Blackwell KN, Zhao A, BR Coleman and GE Haddad (2010). The Role of Protein Kinase A and C Inhibition on Intracellular Calcium Levels during the Development and Regression of Eccentric Cardiac Hypertrophy (In preparation)
GE Haddad, BR Coleman, A Zhao and KN Blackwell (2005). Regulation of myocardial contraction by PKA and PKC during the development and regression of eccentric cardiac hypertrophy. American Journal of Physiology, Feb; 288(2):H695-704.
GE Haddad, BR Coleman, A Zhao and KN Blackwell (2004). Modulation of atrial contraction by PKA and PKC during the compensated phase of eccentric cardiac hypertrophy. Basic Research in Cardiology, v.99: 317-327.
Haddad G., Blackwell K., and A. Bikhazi ((2003). Regulation of IGF-1 by RAS during regression of eccentric hypertrophy through ACE-inhibitor and AT1 antagonist. Canadian Journal of Physiology and Pharmacology, v.81 (2), pp.142-149.
My current research project is focused on understanding the effects of chronic alcohol consumption on beta-adrenergic signaling and its regulation of calcium release during cardiac excitation-contraction coupling. Studies performed using the Lieber-DeCarli alcohol diet in pair-fed Sprague-Dawley rats demonstrates a blunted inotropic response to beta-adrenergic stimulation after 2- and 4- months of alcohol feeding in ventricular cardiomyocytes when compared to its pair-fed control. Experiments to assess cardiac beta-adrenergic receptor function and cyclic adenosine monophosphate (cAMP) levels reveal no change with chronic ethanol consumption. These data suggest that the ?alcoholic? lesion is downstream from cyclic adenosine monophosphate activation and may involve alterations in protein kinase A activation and A-kinase anchoring protein (AKAP) activity. Thus, identifying the effects of chronic alcohol on this signaling pathway may be critical to understanding alterations in cardiac function under stress conditions in alcoholic cardiomyopathy patients.
