2. Academic Validation
  3. High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons

High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons

  • Cell Rep. 2021 Mar 16;34(11):108866. doi: 10.1016/j.celrep.2021.108866.
David I Levi 1,  Joshua C Wyrosdic 1,  Amirah-Iman Hicks 2,  Mary Ann Andrade 3,  Glenn M Toney 3,  Masha Prager-Khoutorsky 4,  Charles W Bourque 5
Affiliations

Affiliations

  • 1 Brain Repair and Integrative Neuroscience Program, Research Institute of the McGill University Health Centre, Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G1A4, Canada.
  • 2 Department of Physiology, McGill University, 3644 Promenade Sir William Osler, Montreal, QC H3G1Y6, Canada.
  • 3 Department of Cellular and Integrative Physiology, University of Texas Health Sciences Centre San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
  • 4 Department of Physiology, McGill University, 3644 Promenade Sir William Osler, Montreal, QC H3G1Y6, Canada. Electronic address: masha.prager-khoutorsky@mcgill.ca.
  • 5 Brain Repair and Integrative Neuroscience Program, Research Institute of the McGill University Health Centre, Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G1A4, Canada. Electronic address: charles.bourque@mcgill.ca.
PMID: 33730577 DOI: 10.1016/j.celrep.2021.108866
Abstract

High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells (MNCVP) that secrete the antidiuretic and vasoconstrictor hormone vasopressin (VP) into the circulation. Here, we show that the intrinsic and synaptic excitation of MNCVP caused by hypertonicity are differentially potentiated in two models of salt-dependent hypertension in rats. One model combined salty chow with a chronic subpressor dose of angiotensin II (AngII-salt), the other involved replacing drinking water with 2% NaCl (salt loading, SL). In both models, we observed a significant increase in the quantal amplitude of EPSCs on MNCVP. However, model-specific changes were also observed. AngII-salt increased the probability of glutamate release by osmoreceptor afferents and increased overall excitatory network drive. In contrast, SL specifically increased membrane stiffness and the intrinsic osmosensitivity of MNCVP. These results reveal that dietary salt increases the excitability of MNCVP through effects on the cell-autonomous and synaptic osmoresponsiveness of MNCVP.

Keywords

angiotensin II; hypertension; mechanosensitivity; osmosensitivity; supraoptic nucleus; vasopressin.

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