My research interests and activities are currently supported by Institutional internal funds, the American Heart Association, and the National Heart, Lung, and Blood Institute of the National Institutes of Health. The funds support research examining mechanisms of expression and cell-surface mobilization of endogenous micro-vascular smooth muscle G protein-coupled α2C-adrenergic receptors (α2C-ARs).

My colleagues and I identified the α2C-ARs as “stress-receptors” of the vascular sympathetic system. We have recently identified a novel signaling cascade in human vascular smooth muscle cells involving cyclic AMP, the Ras-related small G protein Rap1, actin binding protein filamin2, α2C-ARs, and the actin cytoskeleton. Current and future work involves studies to understand the role of Rap1 in the cardiovasculature and examination of stress-induced signature microRNAs and proteins in vascular smooth muscle cells. These studies will potentially lead to identification of physiologically relevant "vasculo-protective" players, conferring "stress-tolerance" to cells during cellular stress or vascular injury.

Broadly, these studies involve understanding the mechanisms behind alterations in peripheral vascular resistance, and peripheral vascular disorders. For example, in the cerebral circulation, in stroke, diabetes, hypercholesterolemia, hypertension, hypothermic response of the microvasculature seen in Raynaud’s phenomenon, secondary Raynaud’s associated with the devastating disease scleroderma, and hand-arm vibration syndrome.