Brayden Lab
We are investigating the ionic mechanisms of vasoconstriction, vasodilation, and communication between endothelial and smooth muscle cells in cerebral arterioles. We are particularly interested in the understanding the mechanisms responsible for the onset and maintenance of intrinsic (myogenic) vascular tone, with special focus on signaling pathways involved in cellular Ca2+ regulation. This work employs state-of-the-art electrophysiological (patch clamp, intracellular electrodes), optical (fluorescence microcopy, arterial diameter recordings), and molecular (gene silencing) techniques. Our recent studies point to important roles for non-selective cation channels as mediators of the depolarization that occurs in vascular smooth muscle cells as intravascular pressure is elevated. Molecular characterization studies demonstrate that these cation channels are members of the Transient Receptor Potential (TRP) channel family. We have also identified TRP family members that contribute to receptor-mediated depolarization and constriction of vascular myocytes. A second area of research in this laboratory is directed towards identifying the roles of the vascular endothelium and its complement of ion channels in cerebral and peripheral artery vasodilator function.
Ion Channels That Regulate [Ca2+]i and Contractile Activity in Cerebral Arterioles
