PMID- 28270592
OWN - NLM
STAT- MEDLINE
DCOM- 20171207
LR  - 20240324
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 5
IP  - 5
DP  - 2017 Mar
TI  - Evidence that remodeling of insular cortex neurovascular unit contributes to 
      hypertension-related sympathoexcitation.
LID - 10.14814/phy2.13156 [doi]
LID - e13156
AB  - The intermediate region of the posterior insular cortex (intermediate IC) 
      mediates sympathoexcitatory responses to the heart and kidneys. Previous studies 
      support hypertension-evoked changes to the structure and function of neurons, 
      blood vessels, astrocytes and microglia, disrupting the organization of the 
      neurovascular unit (NVU). In this study, we evaluated the functional and 
      anatomical integrity of the NVU at the intermediate IC in the spontaneously 
      hypertensive rat (SHR) and its control the Wistar-Kyoto (WKY). Under urethane 
      anesthesia, NMDA microinjection (0.2 mmol/L/100 nL) was performed at the 
      intermediate IC with simultaneous recording of renal sympathetic nerve activity 
      (RSNA), heart rate (HR) and mean arterial pressure (MAP). Alterations in NVU 
      structure were investigated by immunofluorescence for NMDA receptors (NR1), blood 
      vessels (70 kDa FITC-dextran), astrocytes (GFAP), and microglia (Iba1). 
      Injections of NMDA into intermediate IC of SHR evoked higher amplitude responses 
      of RSNA, MAP, and HR On the other hand, NMDA receptor blockade decreased baseline 
      RSNA, MAP and HR in SHR, with no changes in WKY Immunofluorescence data from SHR 
      intermediate IC showed increased NMDA receptor density, contributing to the SHR 
      enhanced sympathetic responses, and increased in vascular density (increased 
      number of branches and endpoints, reduced average branch length), suggesting 
      angiogenesis. Additionally, IC from SHR presented increased GFAP immunoreactivity 
      and contact between astrocyte processes and blood vessels. In SHR, IC microglia 
      skeleton analysis supports their activation (reduced number of branches, 
      junctions, endpoints and process length), suggesting an inflammatory process in 
      this region. These findings indicate that neurogenic hypertension in SHR is 
      accompanied by marked alterations to the NVU within the IC and enhanced 
      NMDA-mediated sympathoexcitatory responses likely contributors of the maintenance 
      of hypertension.
CI  - (c) 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of The Physiological Society and the American Physiological Society.
FAU - Marins, Fernanda R
AU  - Marins FR
AD  - Departamento de Fisiologia e Biofisica, INCT, Instituto de Ciencias Biologicas, 
      Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
FAU - Iddings, Jennifer A
AU  - Iddings JA
AD  - Department of Physiology, Augusta University, Augusta, Georgia.
FAU - Fontes, Marco A P
AU  - Fontes MA
AD  - Departamento de Fisiologia e Biofisica, INCT, Instituto de Ciencias Biologicas, 
      Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
FAU - Filosa, Jessica A
AU  - Filosa JA
AD  - Department of Physiology, Augusta University, Augusta, Georgia 
      jfilosa@augusta.edu.
LA  - eng
GR  - R01 HL089067/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 6384-92-5 (N-Methylaspartate)
SB  - IM
MH  - Animals
MH  - Arterial Pressure/drug effects/physiology
MH  - Astrocytes/metabolism
MH  - Cerebral Cortex/drug effects/*physiology
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Heart Rate/drug effects/physiology
MH  - Hypertension/*physiopathology
MH  - Kidney/*innervation
MH  - N-Methylaspartate/pharmacology
MH  - Neurovascular Coupling/drug effects/*physiology
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Sympathetic Nervous System/drug effects/*physiology
PMC - PMC5350170
OTO - NOTNLM
OT  - Hypertension
OT  - Insular cortex (IC)
OT  - NMDA receptors
OT  - neurovascular unit (NVU)
EDAT- 2017/03/09 06:00
MHDA- 2017/12/08 06:00
PMCR- 2017/03/07
CRDT- 2017/03/09 06:00
PHST- 2017/01/13 00:00 [received]
PHST- 2017/01/18 00:00 [accepted]
PHST- 2017/03/09 06:00 [entrez]
PHST- 2017/03/09 06:00 [pubmed]
PHST- 2017/12/08 06:00 [medline]
PHST- 2017/03/07 00:00 [pmc-release]
AID - 5/5/e13156 [pii]
AID - PHY213156 [pii]
AID - 10.14814/phy2.13156 [doi]
PST - ppublish
SO  - Physiol Rep. 2017 Mar;5(5):e13156. doi: 10.14814/phy2.13156.