Mitsi Blount, PhD

Assistant Professor of Medicine

Department of Medicine

Phone: 404-712-1188

Email: mabloun@emory.edu

Biography

Dr. Blount graduated in 1999 with a BS in biology from the University of North Carolina at Chapel Hill. She earned her PhD in molecular physiology and biophysics at Vanderbilt University School of Medicine in 2005. She was a postdoctoral fellow at Emory University School of Medicine from 2005-2008. Currently, Dr. Blount is a tenure-track assistant professor of medicine in the Department of Medicine's Division of Renal Medicine.

RESEARCH
Intracellular cAMP levels within kidney cells are increased in response to a variety of hormonal and chemical stimuli, including vasopressin. Vasopressin, a hormone released from the pituitary when the body is dehydrated, signals the kidneys to conserve water in order to maintain the body’s water balance. In the inner medullary collecting duct (IMCD), vasopressin increases water permeability allowing for water reabsorption from the tubule lumen thus setting the stage for the production of concentrated urine. Vasopressin binds to the V2 receptor located on the basolateral membrane of the IMCD, activates Gs, which in turn stimulates adenylyl cyclase to synthesize cAMP. The second messenger cAMP has many downstream targets including, 1) cAMP-dependent protein kinase (PKA) and 2) several cAMP-specific phosphodiesterases (PDEs). The exact vasopressin-stimulated cAMP signaling cascade resulting in urine concentration has not been elucidated. Many of the transporters that contribute to urine concentration are in some way mediated by cAMP. One of these transporters is the urea transporter, UT-A1. Our laboratory investigates the many cAMP-mediated processes that regulate UT-A1 function including how vasopressin-stimulated phosphorylation of UT-A1 by PKA effects transporter trafficking and activity. Elucidating the signaling cascades triggered by vasopressin in the IMCD will not only provide new insight into urea handling but may also be beneficial in understanding the mechanisms underlying the disregulation of water homeostasis that occurs in common clinical disorders, such as congestive heart failure, cirrhosis, and nephrotic syndrome.