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Dr. Bryan Slinker's research focuses on heart disease. Many forms of
heart disease result from a "remodeling" of the heart that occurs with
long-standing high blood pressure and following a heart attack. In addition,
many forms of heart disease are said to be "familial" because they have a
genetic basis and occur more frequently in certain families (or within breeds
of dogs, for example). One characteristic of all these forms of heart disease
is that the cells in the heart are able to sense abnormalities in how the
heart interacts with the rest of the body and change their characteristics, or
adapt, to try to change the heart’s ability to pump blood to the body. Much of
how the cells do this sensing is unknown. Similarly, much is unknown about how
the cells modify the characteristics of the heart after they sense an
abnormality, such as high blood pressure. Finally, much more work needs to be
done to understand how the changes in the heart cells that occur with disease
translate into decreased ability of the heart to pump blood.
Through the
generosity of the National Institutes of Health and the American
Heart Association, Dr. Slinker's research has focused on how the heart
regulates its own pumping ability on a minute-to-minute basis, and how this
ability is changed in response to drugs that affect the heart. Much of this
work has been in collaboration with Dr. Ken Campbell. More recently, Dr.
Slinker has begun to study how the heart responds to changes in the mechanical
forces it faces – these forces result from blood pressure and the size and
shape of the heart. This line of study has led to collaboration with Dr.
Joseph Harding. Specifically, they study a hormone system discovered in Dr.
Harding’s lab, called Angiotensin IV. This, and related hormones, are
intimately involved in controlling the changing character of the heart in
disease. In particular, they are interested in how these hormones influence
cells in the heart to secrete proteins that are important in the structure of
the connective tissue, which is "scaffold" that interconnects the cells of the
heart. Many forms of heart disease involve changes in this scaffolding
(sometimes much like scar formation in a cut in your skin) that decrease the
heart’s ability to pump. Understanding how to reverse these changes will
potentially lead to new therapies for heart disease in both humans and
animals.
Biographical Brief
Bryan K. Slinker, Professor and Chair of VCAPP, received
his B.S. in Zoology from the College of Idaho in 1976, and his D.V.M. and
Ph.D. degrees from Washington State University in 1980 and 1982, respectively.
He completed 3-1/2 years of postdoctoral work at the Cardiovascular Research
Institute of the University of California, San Francisco. From 1986-1992, he
was an Assistant Professor in the Department of Medicine (Cardiology Unit) at
the University of Vermont.
Scholarly Publications
Dr. Slinker has more than 50 publications in books and
scientific journals, principally in the American Journal of Physiology,
Circulation Research, Cardiovascular Research, and Journal of
Molecular and Cellular Cardiology. Selected recent publications include:
Yang, Q, JM Hanesworth, JW Harding and BK Slinker:
The AT4 receptor agonist [Nle1] - Angiotensin IV reduces
mechanically induced immediate-early gene expression in the isolated rabbit
heart. Regul. Pept. 71:175-183, 1997
Slinker, BK: The
statistics of synergism. J. Mol. Cell. Cardiol. 30:723-731, 1998
Glantz SA and BK Slinker: Primer of Applied
Regression and Analysis of Variance (2nd ed.). New York,
McGraw-Hill, 2000 (http://www.vetmed.wsu.edu/AppliedRegression/)
Campbell, KB, MV Razumova, RD Kirkpatrick and BK
Slinker: Nonlinear myofilament regulatory processes affect
frequency-dependent muscle fiber stiffness. Biophys J. 81:2278-96, 2001
Campbell,
KB, M Chandra, RD Kirkpatrick, BK Slinker and WC Hunter. Interpreting
cardiac muscle force-length dynamics using a novel functional model. Am J
Physiol 286:H1535-H1545, 2004.
Campbell KB,
Y Wu, AM Simpson, RD Kirkpatrick, SG Shoff, HL Granzier and BK Slinker.
Dynamic myocardial contractile parameters from left ventricular
pressure-volume measurements. Am J Physiol 289:H114-H130, 2005.
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