Ian Bratz, Ph.D.
Assistant Professor of Physiology
Department of Integrative Medical Sciences
College of Medicine
2003: Ph.D., Biomedical Sciences, University of New Mexico, Albuquerque, New Mexico
1998: B.S., Physiology and Chemistry, Michigan State University, East Lansing, Michigan
2008-present: Assistant Professor of Physiology, Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, Ohio
2006-2008: Post-doctoral Fellow, Department of Cellular and Integrative Physiology, IUPUI, Indianapolis, Indiana
2004-2006: Post-doctoral Fellow, Louisiana State University Health Science Center, New Orleans, Louisiana
Having extensive research experience in cardiovascular physiology, I am strongly interested in regulation of vasomotor tone by ion channels expressed in arterial smooth muscle and endothelial cells. Using a varied approach, including patch clamp electrophysiology, molecular biology, laser scanning confocal imaging of intracellular Ca2+ events, and video microscopy recordings of diameter changes in pressurized resistance arteries and antisense-mediated suppression of ion channel expression in intact arteries, my lab examines the role of transient receptor potential (TRP) channels expressed by coronary artery smooth muscle and endothelial cells in vascular function. The TRP channel family is a diverse group of voltage-independent cation channels, ubiquitously expressed that are activated by a broad range of physical, chemical, and environmental stimuli, such as: temperature, pressure, stretch, and fatty acids. Many of its vascular physiological functions remain unclear. The TRPV channels represent one of the six known subfamilies and are characteristically gated by vanilloid compounds (e.g., capsaicin opens TRPV1 channels). Currently, my focus is on elucidating the functional roles of TRPV1 channels in the regulation of coronary vascular tone. Recent studies have implicated various TRPV channels in the regulation of vascular tone, but little is known about the role of TRPV1. Recent data indicate TRPV1 channels are functionally expressed in the coronary circulation and that TRPV1 signaling is disrupted in the metabolic syndrome. Ongoing experiments are focused on elucidating the mechanisms by which TRPV1 channels regulate coronary vascular tone in normal and metabolic syndrome subjects.
Ohanyan VA, Guarini G, Thodeti CK, Talasila PK, Raman P, Haney R, Meszaros JG, Damron DS, Bratz IN. Endothelin Mediated In Vivo Pressor Responses following TRPV1 Activation. Am J Physiol Heart Circ Physiol. 2011 Jun 24. [Epub ahead of print]
Adapala RK, Talasila PK, Bratz IN, Zhang DX, Suzuki M, Meszaros JG, Thodeti CK. PKCα mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells. Am J Physiol Heart Circ Physiol. 2011 Jun 24. [Epub ahead of print]
Zhang H, Wickley PJ, Sinha S, Bratz IN, Damron DS. Propofol restores transient receptor potential vanilloid receptor subtype-1 sensitivity via activation of transient receptor potential ankyrin receptor subtype-1 in sensory neurons. Anesthesiology. 2011 May;114(5):1169-79.
Long X, Bratz IN, Alloosh M, Edwards JM, Sturek M. Short-term exercise training prevents micro- and macrovascular disease following coronary stenting. J Appl Physiol. 2010 Jun;108(6):1766-74.
Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol. 2010 Apr;298(4):H1182-9. 20118408
Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Contribution of BK(Ca) channels to local metabolic coronary vasodilation: Effects of metabolic syndrome. Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H966-73.
Borbouse L, Dick GM, Asano S, Bender SB, Dincer UD, Payne GA, Neeb ZP, Bratz IN, Sturek M, Tune JD. Impaired function of coronary BK(Ca) channels in metabolic syndrome. Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1629-37. Epub 2009 Sep 11.
Edwards JM, Neeb ZP, Alloosh MA, Long X, Bratz IN, Peller CR, Byrd JP, Kumar S, Obukhov AG, Sturek M. Exercise training decreases store-operated Ca2+entry associated with metabolic syndrome and coronary atherosclerosis. Cardiovasc Res. 2010 Feb 1;85(3):631-40. Epub 2009 Sep 10.
Payne GA, Borbouse L, Bratz IN, Roell WC, Bohlen HG, Dick GM, Tune JD. Endogenous adipose-derived factors diminish coronary endothelial function via inhibition of nitric oxide synthase. Microcirculation. 2008. July;15 (5):417-26.
Bratz IN, Dick GM, Tune JD, Edwards JM, Neeb ZP, Dincer UD, Sturek M. Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome. Am J Physiol Heart Circ Physiol. 2008; 294(6);H2489-96.
Dick GM, Bratz IN, Borbouse L, Payne GA, Dincer UD, Knudson JD, Rogers PA, Tune JD. Voltage dependent K+ channels regulate the duration of reactive hyperemia in canine coronary circulation. Am J Physiol Heart Circ Physiol. 2008 May:294(5):H2371-81.
Knudson JD, Dincer UD, Bratz IN, Sturek M, Dick GM, Tune JD. Mechanisms of Coronary dysfunction in obesity and insulin resisitance. Microcirculation. 2007 June-July; 14(4-5): 317-38.
Rogers PA, Chilian WM, Bratz IN, Bryan RM, Dick GM. H202 activates redox- and 4-aminopyridine sensitive KV channels in coronary vascular smooth muscle. Am J Physiol Heart Circ Physiol 292(3):H1404-11, 2007.
Rogers PA, Dick GM, Knudson JD, Focardi M, Bratz IN, Swafford Jr AN, Saitoh S, Tune JD, Chilian WM. H202 induced redox-sensitive coronary vasodilation is mediated by 4-aminopyridine-sensitive K+ channels. Am J Physiol Heart Circ Physiol 291(5):H2473-82, 2006.
Knudson, JD, Rogers PA, Dincer UD, Bratz IN, Araiza AG, Dick GM, Tune JD. Coronary Vasomoter Reactivity to Endothelin-1 in the Prediabetic Metabolic Syndrome. Microcirculation 2006; 13: 209-218.
Bratz IN, Swafford AN, Kanagy NL, Dick GM. Reduced functional expression of K+ channels in vascular smooth muscle cells from rats made hypertensive with N-ϖ-nitro-L-arginine. Am J Physiol (Heart Circ Physiol) 2005; Sep; 289(3):H1284-90.
Bratz IN, Dick GM, Partridge LD, Kanagy NL. Reduced molecular expression of K+ channels in vascular smooth muscle cells from rats made hypertensive with N-ϖ-nitro-L-arginine. Am J Physiol (Heart Circ Physiol) 2005; Sep; 289(3):H1277-83.
Swafford AN, Bratz IN, Knudson JD, Rogers PA, Timmerman JM, Tune JD, Dick GM. C-reactive protein does not relax vascular smooth muscle: effects mediated by sodium azide in commercially available preparations. Am J Physiol (Heart Circ Physiol) 2005; Apr; 228(4): H1786-95.
Bratz IN and Kanagy NL. Nitric oxide synthase-inhibition is associated with altered endothelial cyclooxygenase function. Am J Physiol (Heart Circ Physiol) 2004; 287(6):H2394-401.
Bratz IN, Falcon RF, Partridge LD, Kanagy NL. Vascular smooth muscle cell membrane depolarization following NOS-inhibition hypertension. Am J Physiol (Heart Circ Physiol) 2002; 282:H1648-55.