KENNETH SPITZER
Professor of Physiology
e-mail: spitzer@cvrti.utah.edu
Education
BA, Virginia Military Institute, Lexington, Virginia, 1966, Biology
MS, Virginia Polytechnic Institute, Blacksburg, Virginia, 1968, Zoology
PhD, State University of New York School of Medicine, Buffalo, New York, 1977, Physiology Postdoctoral Fellow, Department of Physiology, University of Utah, Salt Lake City, Utah, 1977-79
Research Interests
Cardiac Intracellular pH Regulation. One project focuses on the sarcolemmal ion transport systems that control the intracellular acid-base status of cardiac cells. The experiments are designed to examine the modulatory influence of vasoactive peptides on pH control systems. The experiments are performed on single cardiac myocytes using either conventional epifluoresence techniques or confocal imaging. Other studies are designed to evaluate intra- and extracellular diffusion of protons.
Electrical Interactions Between Cardiac Cells. This research is designed to better understand how electrical communications between individual cardiac cells affects action potential characteristics, intracellular Ca and contraction. The approach is to electrically connect two physically separate cardiac myocytes through an electronic circuit that allows for variation in electrical resistance between the two cells, thus simulating variations in normal gap junctional resistance.
Cardiac Excitation - Contraction Coupling. This research focuses on the relationship between electrical events in the sarcolemma and intracellular Ca regulation. Of current interest is the mechanism of Ca regulation in cardiac Purkinje cells. These cells lack transverse tubules and have uniquely shaped action potentials. The experiments are performed on isolated Purkinje myocytes using patch clamp techniques and confocal imaging of intracellular calcium.
Publications
(Go to the complete list in PDF Format.)
Spitzer, K.W., Skolnick, R.L., Peercy, B.E.k Keener, J.P. and Vaughan-Jones, R.D. (2002) Facilitation of intracellular H+ ion mobility by CO2/HCO3 in rabbit ventricular myocytes is regulated by carbonic anhydrase. J. Physiol. (London) 541: 159-167.
Vaughan-Jones, R.D., Peercy, B.E., Keener, J.P. and Spitzer, K.W. (2002) Intrinsic H+ ion mobility in the rabbit ventricular myocyte. J. Physiol. (London) 541: 139-158.
Su, Z., Sugishita, K., Ritter, M., Li, F., Spitzer, K.W. and Barry, W.H. (2001) The sodium pump modulates the influence of I(Na) on [Ca2+]i transients in mouse ventricular myocytes. Biophys. J. 80(3): 1230-1237.
Cordeiro, J.M., Bridge, J.H.B. and Spitzer, K.W. (2001) Early and delayed afterdepolarizations in rabbit heart Purkinje cells viewed by confocal microscopy. Cell Calcium 29(5): 289-297.
Cordeiro, J.M., Spitzer, K.W., Giles, W.R., Ershler, P.E., Cannell, M.B. and Bridge, J.H.B. (2001) Location of the initiation site of calcium transients and sparks in rabbit heart Purkinje cells. J. Physiol. (London) 531: 301-314.
Huelsing, D.J., Pollard, A.E. and Spitzer, K.W. (2001) Transient outward current modulates discontinuous conduction in rabbit ventricular cell pairs. Cardiovascular Research 49: 769-779.
Huelsing, D.J., Spitzer, K.W. and Pollard, A.E. (2000) Electrotonic suppresion of early afterdepolarizations in isolated rabbit Purkinje myocytes. Am. J. Physiol. Heart Circ. Physiol. 279: H250-H259.
Ritter, M., Su, Z., Spitzer, K.W., Ishida, H. and Barry, W.H. (2000) Caffeine-induced Ca2+ sparks in mouse ventricular myocytes. Am. J. Physiol. Heart Circ. Physiol. 278: H666-H669.
Spitzer, K.W., Ershler, P.R., Skolnick, R.L. and Vaughan-Jones, R.D. (2000) Generation of intracellular pH gradients in single cardiac myocytes with a microperfusion system. Am. J. Physiol. Heart Circ. Physiol. 278: H1371-H1382.
Zaniboni, M., Pollard, A.E., Yang, L. and Spitzer, K.W. (2000) Beat-to-beat repolarization variability in ventricular myocytes and its suppression by electrical coupling. Am. J. Physiol. Heart Circ. Physiol. 278: H677-H687.
Zu, Z., Bridge, J.H.B., Philipson, K.D., Spitzer, K.W. and Barry, W.H. (1999) Quantitation of Na/Ca exchanger function in single ventricular myocytes. J. Mol. Cell. Cardiol. 31: 1125-1135.
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