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Michael A. Hill, PhD

Associate Director, Dalton Cardiovascular Research Center
Professor, Department of Medical Pharmacology and Physiology
 Office Location: 133A Dalton Cardiovascular Research Center
Office Phone: 573-884-4601
HillMi@missouri.edu

Research Interests

  • Microcirculation
  • Vascular Smooth Muscle
  • Ca2+
  • Ion Channels
  • Imaging
  • Vascular Complications of Diabetes

Research Description

Our laboratory has a principal interest in understanding the signaling mechanisms that underlie the vasoconstrictor response of an arteriole following an acute rise in intraluminal pressure (myogenic response). Broadly speaking this can be considered as a process of mechanotransduction. Our studies have examined the roles of a number of vascular smooth muscle signaling molecules including various kinases and intracellular Ca2+. More recently these studies have been extended to include approaches aimed at determining the relationships between pressure-induced changes in smooth muscle membrane potential, sub-cellular Ca2+ signaling, and the resulting signaling events that ultimately lead to the contractile response.

In addition to basic studies on myogenic signaling we are also studying how myogenic tone interacts with other vasoregulatory mechanisms (principally, endothelial-dependent dilation) and how the myogenic response is altered in diabetes mellitus.

Professional Background

  • Obtained PhD, University of Melbourne.
  • Completed postdoctoral training at Department of Medical Physiology, Texas A&M University.
  • Received Fulbright Fellowship in 1988.
  • Received National Institutes of Health (NIH) FIRST Award in 1992.
  • Obtained past funding from NIH, Juvenile Diabetes Foundation, American Heart Association, National Health and Medical Research Council (Australia); National Heart Foundation (Australia).
  • Acts as a current member of American Heart Foundation (National) grant review panel.
  • Acts as a member of editorial boards of Microcirculation (present), Journal of Vascular Research (present) and American Journal of Physiology (1996-98).

Selected Publications

  • Davis, M.J. and Hill, M.A. Signaling mechanisms underlying the vascular myogenic response. Physiological Reviews 79:387-423, 1999.
  • Zou, H., Ratz, P.H. and Hill, M.A. Temporal aspects of [Ca2+]i and myosin phosphorylation during myogenic and agonist-induced arteriolar constriction. J. Vasc. Res. 37:556-567, 2000.
  • Murphy, T.V., Spurrell, B.E. and Hill, M.A. Tyrosine kinase activity following alterations in intraluminal pressure and wall tension in rat cremaster arterioles. Am. J. Physiol. 281:H1047-H1056, 2001.
  • Hill, M.A., Zou, H., Potocnik, S.J., Meininger, G.A. and Davis, M.J. Arteriolar smooth muscle mechanotransduction: Ca2+ signaling underlying myogenic reactivity. J. App. Physiol. 91:973-983, 2001.
  • Bishara, N., Dunlop, M.E., Murphy, T.V., Darby, I.A., Rajanayagam, M.A.S.and Hill, M.A. Matrix protein glycation impairs agonist-induced intracellular Ca2+ signaling in endothelial cells. J. Cell Physiol. 193:80-92, 2002. January 28, 2008
  • M.A. Increased intraluminal pressure stimulates MAP kinase phosphorylation in arterioles: dissociation from the acute myogenic contractile response. Am. J. Physiol. 285:H1764-73, 2003.
  • Martinez-Lemus, L.A., Hill, M.A., Bolz, S.S., Pohl, U. and Meininger, G.A. Vascular Smooth Muscle Cell Slipping and Creeping: An acute form of vascular remodeling. FASEB J. 18:708-10, 2004.
  • Kotecha, N. and Hill, M.A. Arteriolar smooth muscle membrane potential and Ca2+i supply during myogenic contraction of skeletal muscle arterioles. Am. J. Physiol. 289:H1326-1334, 2005.
  • Bishara, N.V., Triggle, C.R. and Hill, M.A.  Relationship between store-operated and arachidonic acid sensitive Ca2+ entry in endothelial cells.  Endothelium 12:153-161, 2005.
  • Hill, M.A., Davis, M.J., Meininger, G.A., Potocnik, S.J. and Murphy, T.V. Arteriolar myogenic signalling mechanisms: Implications for local vascular function. Clin. Haemorrheol. Microcirc. 34:67-79, 2006.
  • McSherry, I. N., Sandow, S. L., Campbell, W. B., Falck, J. R., Hill, M. A. and Dora, K. A. A role for heterocellular coupling and EETs in dilation of rat cremaster arteries. Microcirculation 13:119-130, 2006.
  • Potocnik, S.J., Jenkins, N., Murphy, T.V. and Hill, M.A. Membrane cholesterol depletion with b-cyclodextrin impairs calcium signalling and pressure-induced contraction in isolated skeletal muscle arterioles.  J. Vasc. Res.44:292-302, 2007.
  • Murphy, T.V., Kotecha, N. Hill, M.A. Endothelium-independent constriction of isolated, pressurized arterioles by Nw-nitro-L-arginine methyl ester (L-NAME). Br. J. Pharmacol. 151:602-609, 2007.
  • Hill, M.A., Sun, Z., Martinez-Lemus, L. and Meininger, G.A.  Novel imaging approaches provide a driving force to advance the field of arteriolar and vascular cell mechanotransduction. Trends in Pharmacol. Sci. 28:308-315, 2007. 
  • Hill, M.A. and Davis, M.J. Coupling a Change in Intraluminal Pressure to Vascular Smooth Muscle Depolarization: Still Stretching for an Explanation. (Editorial Focus) Am. J. Physiol. 292:H2570-H2572, 2007.
  • Kockx, M., Guo, D.L., Kay, J., Saba, M., Jary, E., Hill, M.A., Gaus, K., Stow, J., Jessup, W. and Kritharides, L. Secretion of apolipopotein E from human macrophages occurs via a protein kinase A- and calcium-dependent pathway along the microtubule network. Circ. Res. 101:607-616, 2007.
  • Davis, M.J., Hill, M.A. and Kuo, L. Regulation of Microvascular Blood Flow, in Microcirculation, Handbook of Physiology (2nd Edition), Eds Tuma, Duran and Ley, Academic Press, 2008, Ch 6, pp161 – 285.
  • Raina, H., Ella, S.R. and Hill, M.A. Decreased expression of the smooth muscle Na+/Ca2+ exchanger impairs arteriolar myogenic reactivity. J. Physiol. 586:1669-1681, 2008.
  • Young, E.J., Hill, M.A., Wiehler, W.B., Triggle, C.R., and Reid, J.J. Reduced EDHF responses and connexin activity in mesenteric arteries from the insulin-resistant obese Zucker rat.  Diabetologia 51:872-881, 2008.
  • Sun, Z., Martinez-Lemus, L.A., Hill, M.A. and Meininger, G.A. Extracellular matrix specific focal adhesions in vascular smooth muscle produce mechanically active adhesion sites.  Am. J. Physiol. Cell Physiol. 295:C268-C278, 2008.

  • Sheng, J-Z, Ella, S.R., Davis, M.J., Hill, M.A. and Andrew P. Braun Openers of small and intermediate-conductance, Ca2+-activated K+ channels enhance agonist-evoked endothelial nitric oxide synthesis and vasodilation of rat cremaster arterioles. FASEB J.  In Press (Nov), 2008.

Published by Dalton Cardiovascular Research Center, 134 Research Park Dr., Columbia, MO 65211
Phone: 573-882-7588 | Fax: 573-884-4232 | Email: dalton@missouri.edu
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