PMID- 28428739
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240325
IS  - 1662-4548 (Print)
IS  - 1662-453X (Electronic)
IS  - 1662-453X (Linking)
VI  - 11
DP  - 2017
TI  - High Salt Intake Augments Excitability of PVN Neurons in Rats: Role of the 
      Endoplasmic Reticulum Ca(2+) Store.
PG  - 182
LID - 10.3389/fnins.2017.00182 [doi]
LID - 182
AB  - High salt (HS) intake sensitizes central autonomic circuitry leading to 
      sympathoexcitation. However, its underlying mechanisms are not fully understood. 
      We hypothesized that inhibition of PVN endoplasmic reticulum (ER) Ca(2+) store 
      function would augment PVN neuronal excitability and sympathetic nerve activity 
      (SNA). We further hypothesized that a 2% (NaCl) HS diet for 5 weeks would reduce 
      ER Ca(2+) store function and increase excitability of PVN neurons with axon 
      projections to the rostral ventrolateral medulla (PVN-RVLM) identified by 
      retrograde label. PVN microinjection of the ER Ca(2+) ATPase inhibitor 
      thapsigargin (TG) increased SNA and mean arterial pressure (MAP) in a 
      dose-dependent manner in rats with a normal salt (NS) diet (0.4%NaCl). In 
      contrast, sympathoexcitatory responses to PVN TG were significantly (p < 0.05) 
      blunted in HS treated rats compared to NS treatment. In whole cell current-clamp 
      recordings from PVN-RVLM neurons, graded current injections evoked graded 
      increases in spike frequency. Maximum discharge was significantly augmented (p < 
      0.05) by HS diet compared to NS group. Bath application of TG (0.5 muM) increased 
      excitability of PVN-RVLM neurons in NS (p < 0.05), yet had no significant effect 
      in HS rats. Our data indicate that HS intake augments excitability of PVN-RVLM 
      neurons. Inhibition of the ER Ca(2+)-ATPase and depletion of Ca(2+) store likely 
      plays a role in increasing PVN neuronal excitability, which may underlie the 
      mechanisms of sympathoexcitation in rats with chronic HS intake.
FAU - Larson, Robert A
AU  - Larson RA
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
FAU - Chapp, Andrew D
AU  - Chapp AD
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
FAU - Gui, Le
AU  - Gui L
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
AD  - Department of Cardiology, Affiliated Hospital of Nantong UniversityNantong, 
      China.
FAU - Huber, Michael J
AU  - Huber MJ
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
FAU - Cheng, Zixi Jack
AU  - Cheng ZJ
AD  - Biomolecular Science Center, Burnett School of Biomedical Sciences, College of 
      Medicine, University of Central FloridaOrlando, FL, USA.
FAU - Shan, Zhiying
AU  - Shan Z
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
FAU - Chen, Qing-Hui
AU  - Chen QH
AD  - Department of Kinesiology and Integrative Physiology, Michigan Technological 
      UniversityHoughton, MI, USA.
LA  - eng
GR  - R15 HL122952/HL/NHLBI NIH HHS/United States
GR  - R15 HL145655/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20170406
PL  - Switzerland
TA  - Front Neurosci
JT  - Frontiers in neuroscience
JID - 101478481
PMC - PMC5382644
OTO - NOTNLM
OT  - endoplasmic reticulum
OT  - high salt diet
OT  - hypertension
OT  - paraventricular nucleus
OT  - sympathetic nerve activity
EDAT- 2017/04/22 06:00
MHDA- 2017/04/22 06:01
PMCR- 2017/01/01
CRDT- 2017/04/22 06:00
PHST- 2017/01/29 00:00 [received]
PHST- 2017/03/20 00:00 [accepted]
PHST- 2017/04/22 06:00 [entrez]
PHST- 2017/04/22 06:00 [pubmed]
PHST- 2017/04/22 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fnins.2017.00182 [doi]
PST - epublish
SO  - Front Neurosci. 2017 Apr 6;11:182. doi: 10.3389/fnins.2017.00182. eCollection 
      2017.