22 Jan Brain Functions May Be Affected By Chronic High Salt Intake
Medical Research: What is the background for this study? What are the main findings?
Dr. Bourque: Previous work has established that there is a link between a high level of dietary salt intake and the development of hypertension. In particular, so-called “salt-sensitive” individuals display increases in blood pressure that correlate with significantly increased levels of serum sodium concentration. Increased sodium levels are known to cause an excitation of vasopressin (VP)-releasing neurons of the hypothalamus. We therefore tested the hypothesis that this increase can contribute to the increase in blood pressure associated with high sodium intake in rats.
Medical Research: What should clinicians and patients take away from your report?
Dr. Bourque: Our study shows that a high degree of salt ingestion can cause significant biochemical changes within the brain that can alter the balance between well-defined excitatory and inhibitory circuits in a manner that leads to impaired centrally-mediated homeostasis and cardiovascular pathology. When it comes to hypertension, much of the focus has been placed previously on peripheral factors such as vasomotor tone, vascular resistance and renal deficits. Our work shows that changes in the function of brain circuits can also play an important role in this disease. Changes in central function associated with salt intake may go beyond those we discovered in the VP neurons of the hypothalamus. It is therefore possible that other brain functions may be affected by chronic high salt intake.
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Bourque: First and foremost, we must determine if similar changes can be observed in patients identified as salt-sensitive individuals. There are well-established protocols for testing sodium-sensitive and baroreceptor pathways in humans, so this is a goal that is possible in the near term.
Second, it will be important to investigate if these effects can be fully reversed by lowering salt intake and, if so, determine if individuals become sensitized to subsequent exposures to salt.
Lastly, experiments on animals should increase our understanding of the biochemical mechanisms that link serum sodium levels to KCC2 expression in VP neurons, and determine of other central processes are affected by high salt intake.
Katrina Y. Choe, Su Y. Han, Perrine Gaub, Brent Shell, Daniel L. Voisin, Blayne A. Knapp, Philip A. Barker, Colin H. Brown, J. Thomas Cunningham, Charles W. Bourque. High Salt Intake Increases Blood Pressure via BDNF-Mediated Downregulation of KCC2 and Impaired Baroreflex Inhibition of Vasopressin Neurons. Neuron, 2015; DOI: 10.1016/j.neuron.2014.12.048