Masha Prager-Khoutorsky1, Katrina Y Choe2, David I Levi3, Charles W Bourque4. 1. Department of Physiology, McGill University, McIntyre Medical Sciences Bldg., 3655 Promenade Sir-William Osler, Montreal, QC, H3G 1Y6, Canada. 2. 2309 Gonda Neuroscience and Genetics Research Center, UCLA Department of Neurology, 695 Charles E. Young Dr. South, Los Angeles, CA, 90095, USA. 3. Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC, H3G 1A4, Canada. 4. Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC, H3G 1A4, Canada. charles.bourque@mcgill.ca.
Abstract
PURPOSE OF REVIEW: Dietary salt intake increases both plasma sodium and osmolality and therefore increases vasopressin (VP) release from the neurohypophysis. Although this effect could increase blood pressure by inducing fluid reabsorption and vasoconstriction, acute activation of arterial baroreceptors inhibits VP neurons via GABAA receptors to oppose high blood pressure. Here we review recent findings demonstrating that this protective mechanism fails during chronic high salt intake in rats. RECENT FINDINGS: Two recent studies showed that chronic high sodium intake causes an increase in intracellular chloride concentration in VP neurons. This effect causes GABAA receptors to become excitatory and leads to the emergence of VP-dependent hypertension. One study showed that the increase in intracellular chloride was provoked by a decrease in the expression of the chloride exporter KCC2 mediated by local secretion of brain-derived neurotrophic factor and activation of TrkB receptors. Prolonged high dietary salt intake can cause pathological plasticity in a central homeostatic circuit that controls VP secretion and thereby contribute to peripheral vasoconstriction and hypertension.
PURPOSE OF REVIEW: Dietary salt intake increases both plasma sodium and osmolality and therefore increases vasopressin (VP) release from the neurohypophysis. Although this effect could increase blood pressure by inducing fluid reabsorption and vasoconstriction, acute activation of arterial baroreceptors inhibits VP neurons via GABAA receptors to oppose high blood pressure. Here we review recent findings demonstrating that this protective mechanism fails during chronic high salt intake in rats. RECENT FINDINGS: Two recent studies showed that chronic high sodium intake causes an increase in intracellular chloride concentration in VP neurons. This effect causes GABAA receptors to become excitatory and leads to the emergence of VP-dependent hypertension. One study showed that the increase in intracellular chloride was provoked by a decrease in the expression of the chloride exporter KCC2 mediated by local secretion of brain-derived neurotrophic factor and activation of TrkB receptors. Prolonged high dietary salt intake can cause pathological plasticity in a central homeostatic circuit that controls VP secretion and thereby contribute to peripheral vasoconstriction and hypertension.
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