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Kenneth
L. Byron, Ph.D. Vascular smooth muscle (VSM) cells form a layer of contractile tissue in blood vessel walls. Coordinated contraction or relaxation of these cells determines the vessel diameter and thereby influences the flow of blood through the lumen of the vessel. The contractile state of VSM is regulated primarily by the intracellular calcium ion concentration ([Ca2+]i). An increase in [Ca2+]i leads to activation of myosin-light chain kinase, myosin phosphorylation, and ultimately to an increase in contraction. Physiologically, an increase in [Ca2+]i may occur in response to circulating or locally released hormones or neurotransmitters that bind to cell surface receptors. Binding is then transduced into an increase in Ca2+ influx across the cell’s outer membrane (plasma membrane) and/or a release of intracellular Ca2+ stores. Hormone-induced Ca2+ signals are important both for contraction and for initiation of cell proliferation, though these two physiological responses may require different Ca2+ signals that occur over different ranges of hormone concentration (Byron, 1996). Dr. Byron's laboratory has identified a novel mechanism for the action of the vasoconstrictor hormone, vasopressin, which leads to an increase in the frequency of action potentials in VSM. Action potentials are electrical signals that trigger an influx of calcium across the cell's plasma membrane. His laboratory utilizes a multifaceted experimental program, including molecular, biochemical, and cell physiological approaches designed to identify the molecules involved in the regulatory mechanisms and their functional roles in cell physiology. In addition, experiments using isolated arterial segments and in vivo measurements of arterial vasomotion, blood flow, and blood pressure provide a more complete understanding of how these mechanisms function at the tissue and whole animal levels. View a partial list of Dr. Byron's publications through the National Library of Medicine's PubMed online database.
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