Michael A. Hill, Ph.D.

Professor HillMi@missouri.edu

Research Interests

Our laboratory has a principal interest in understanding the signalling mechanisms that underlie the vasoconstrictor response of an arteriole following an acute rise in intraluminal pressure (myogenic response). Our studies have examined the roles of a number of vascular smooth muscle signalling 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 and the resulting signalling events that ultimately lead to the contractile response.

In addition to basic studies on myogenic signalling 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

• PhD University of Melbourne, Australia, 1988
• Postdoctoral training at Department of Medical Physiology, Texas A&M University 1988-1991
• Fulbright Fellowship 1988
• Past Funding: NIH, Juvenile Diabetes Foundation, American Heart Association, National
• Health and Medical Research Council (Australia); National Heart Foundation (Australia).

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.
• Spurrell, B.E., Murphy, T.V. and Hill, 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
• 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.

Methodology/Techniques

In vitro study of single cannulated arterioles; in vivo study of arterioles within a vascular network; fluorescence microscopy; image analysis; measurement of membrane potential using glass electrodes and fluorescence resonance energy transfer (FRET); cellular approaches including electrophoresis/western transfer, immunohistochemistry and real time PCR.