Dr. Thomas Pallone is Professor of Medicine in the Division of Nephrology. He received the medical degree at Pennsylvania State University followed by Internal Medicine residency training at the University of Maryland, Nephrology fellowship training at Stanford University and additional research training in the Medical Engineering Medical Sciences division of the HST program at the Massachusetts Institute of Technology.
Research in my laboratory involves study of the physiology of renal medullary microcirculation. There have been three foci.
The first line of investigation has been microvascular transport by the medullary microcirculation. That area addresses countercurrent exchange in the renal medulla relevant to the urinary concentrating mechanism. Ongoing studies in this area are now focused on transport processes between cells of the vessels wall through connexins. We have found that the endothelial layer is an electrical syncytium that is capable of transporting large molecules between cells along the vessel axis. The latter is relevant to microvascular contraction and endothelium dependent vasodilator functions.
A second area of emphasis has been the control of vasoactivity of descending vasa recta ~12 to 20 micron diameter microvessels that supply all blood flow to the renal medulla. Areas of study include the role of membrane potential as a regulator of calcium entry into smooth muscle / pericytes and endothelial cells and the ion channel architecture that controls it. We have studied the role of reactive oxygen species and oxidative stress in the regulation of vasoactivity in both health and hypertension.
A third area of investigation control of renal medullary perfusion and renal microvessel function by cardiac glycosides such as ouabain. That topic has been pursued in collaboration with investigators in the Department of Physiology, headed by Dr. Mordecai Blaustein. Our investigations have shown that ouabain modulates Ca2+ signaling and nitric oxide generation by the endothelium. We have found that chronic ouabain elevation induces hypertension and leads to diminution of endothelial nitric oxide generation.