Putative Mechanism of Salt-Dependent Neurogenic Hypertension: Cell-Autonomous Activation of Organum Vasculosum Laminae Terminalis Neurons by Hypernatremia.

@article{Guyenet2017PutativeMO,
  title={Putative Mechanism of Salt-Dependent Neurogenic Hypertension: Cell-Autonomous Activation of Organum Vasculosum Laminae Terminalis Neurons by Hypernatremia.},
  author={Patrice G Guyenet},
  journal={Hypertension},
  year={2017},
  volume={69 1},
  pages={20-22}
}
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. In conscious humans, hyperosmotic stimuli elevate blood pressure (BP) and sympathetic tone, and this particular neurogenic response likely contributes to salt-dependent… CONTINUE READING

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The inward ( depolarizing ) current produced by raising [ NaCl e ] in vitro persisted under conditions of reduced synaptic transmission ( tetrodotoxin plus blockers of ionotropic glutamate and GABA receptors ) , suggesting that OVLT neurons could be intrinsically sensitive to hypernatremia .
The inward ( depolarizing ) current produced by raising [ NaCl e ] in vitro persisted under conditions of reduced synaptic transmission ( tetrodotoxin plus blockers of ionotropic glutamate and GABA receptors ) , suggesting that OVLT neurons could be intrinsically sensitive to hypernatremia .
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 .
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 .
In the SFO , Na sensing requires a sodium channel ( Na x , SCN7a ) that is distantly related to the family of voltage - activated channels responsible for action potential generation in neurons but neither voltage operated not tetrodotoxin sensitive .
Sodium ChlorideContraindicated with diseaseHypernatremia
The inward ( depolarizing ) current produced by raising [ NaCl e ] in vitro persisted under conditions of reduced synaptic transmission ( tetrodotoxin plus blockers of ionotropic glutamate and GABA receptors ) , suggesting that OVLT neurons could be intrinsically sensitive to hypernatremia .
Kinsman et al demonstrate that in tissue slices , 56% of OVLT neurons are vigorously activated by low - grade hyperosmotic hypernatremia ( 2.5–10 mmol / L increase in [ NaCl e ] ) .
Regardless of the precise mechanism by which hyperosmotic hypernatremia activates OVLT neurons , a key question addressed by Kinsman et al is whether these neurons respond to physiologically relevant changes in plasma [ NaCl ] in vivo .
In this issue of Hypertension , Kinsman et al 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 inward ( depolarizing ) current produced by raising [ NaCl e ] in vitro persisted under conditions of reduced synaptic transmission ( tetrodotoxin plus blockers of ionotropic glutamate and GABA receptors ) , suggesting that OVLT neurons could be intrinsically sensitive to hypernatremia .
In the SFO , Na sensing requires a sodium channel ( Na x , SCN7a ) that is distantly related to the family of voltage - activated channels responsible for action potential generation in neurons but neither voltage operated not tetrodotoxin sensitive .
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