The main research focus of Dr. Thomas’ lab is to understand the role of the sympathetic nervous system in the control of cardiovascular function during physiologically stressful situations such as exercise, as well as during pathophysiological conditions such as heart failure and muscular dystrophy. Our ongoing research projects include: (1) elucidating the local mechanisms that modulate sympathetic vasoconstriction in exercising skeletal muscle with a recent focus on nitric oxide and reactive oxygen species; (2) determining the role of estrogen and estrogen receptors in the sympathetic control of cardiovascular function during exercise; and (3) investigating a role for ischemia in the pathogenesis of skeletal muscle degeneration and cardiac dysfunction that occur in muscular dystrophy. We perform studies using a variety of animal models including rats and genetically-engineered mice as well as in human subjects, with the goal of translating the findings from our basic science and experimental animal research into the clinical understanding of integrative cardiovascular control in health and disease.
RESEARCH INTERESTS
Sympathetic neural control of the cardiovascular system during exercise
Local modulation of adrenergic vasoconstriction in skeletal muscle
Estrogen and cardiovascular function
Cardiovascular pathophysiology in muscular dystrophy
RECENT PUBLICATIONS
Fadel P.J., Zhao W., and Thomas G.D, "Impaired vasomodulation is associated with reduced neuronal nitric oxide synthase in skeletal muscle of ovariectomized rats" J. Physiol., 549:243-253, 2003
Thomas GD and Segal SS, "Neural control of muscle blood flow during exercise" J. Appl. Physiol., 97:731-8, 2004
Fadel PJ, Wang Z, Watanabe H, Arbique D, Vongpatanasin W, and Thomas GD, "Augmented sympathetic vasoconstriction in exercising forearms of postmenopausal women is reversed by oestrogen therapy" J. Physiol., 561:893-901, 2004
Lambert DG and Thomas GD, "Alpha-adrenoceptor constrictor responses and their modulation in slow-twitch and fast-twitch mouse skeletal muscle" J. Physiol., 563:821-9, 2005
SIGNIFICANT PUBLICATIONS
Thomas G.D., Shaul P.W., Yuhanna I.S., Froehner S.C., and Adams M.E., "Vasomodulation by skeletal muscle-derived nitric oxide requires alpha-syntrophin-mediated sarcolemmal localization of neuronal nitric oxide synthase" Circ. Res., 92:554-560, 2003
Fadel P.J., Wang Z., Tuncel M., Watanabe H., Abbas A., Arbique D., Vongpatanasin W., Haley R.W., Victor R.G., and Thomas G.D., "Reflex sympathetic activation during static exercise is severely impaired in patients with myophosphorylase deficiency" J. Physiol., 548:983-993, 2003
Thomas G.D., Hansen J., and Victor R.G., "ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle" J. Clin. Invest., 99:2602-2609, 1997
Thomas G.D., Sander M., Lau K.S., Huang P.L., Stull J.T., and Victor R.G., "Impaired metabolic modulation of alpha-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle" Proc. Natl. Acad. Sci., 95:15090-15095, 1998
Sander M., Chavoshan B., Harris S.A., Iannoccone S.T., Stull J.T., Thomas G.D., and Victor R.G., "Functional muscle ischemia in neuronal NOS-deficient skeletal muscle of children with Duchenne muscular dystrophy" Proc. Natl. Acad. Sci., 97:13818-13823, 2000
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