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See related article, pp 163–170 Hypernatremia elicits multiple adaptive responses mediated via the central nervous system: the sensation of thirst, drinking (seeking and consuming fluids), changes in taste preference (water versus salt), and neuroendocrine responses that affect the circulatory system along with sodium and water excretion by the kidneys.1 In conscious humans, hyperosmotic stimuli elevate blood pressure (BP) and sympathetic tone,2 and this particular neurogenic response likely contributes to salt-dependent hypertension. In this issue of Hypertension , Kinsman et al3 suggest that the autonomic nervous system effects elicited by systemic hypernatremia result from a direct action of [NaCl] on neurons located within the organum vasculosum laminae terminalis (OVLT).The OVLT along with the subfornical organ (SFO) and the median preoptic nucleus (MnPO) is an interconnected structure that line the anterior wall of the third ventricle (Figure) and orchestrate the behavioral and autonomic responses to hyperosmolarity.4 The SFO and OVLT detect and encode the concentration of sodium present in the brain extracellular space and possibly the cerebrospinal fluid. They have fenestrated capillaries that facilitate sodium equilibration between plasma and brain extracellular fluid and render their neuropil accessible to circulating hormones, such as angiotensin II. The MnPO bridges the SFO and OVLT (Figure) and probably also contain sodium and osmotic pressure sensors; this imperfectly defined structure is a crucial integrative center for sodium and fluid homeostasis.5,6Figure. Organum vasculosum laminae terminalis (OVLT) and salt-sensitive neurogenic hypertension. Hypernatremia activates OVLT neurons directly or via local astrocytes. OVLT activation augments muscle sympathetic nerve activity (SNA) and reduces renal SNA, thereby …

Putative Mechanism of Salt-Dependent Neurogenic Hypertension