PMID- 18722165
OWN - NLM
STAT- MEDLINE
DCOM- 20090122
LR  - 20211020
IS  - 1872-7484 (Electronic)
IS  - 1566-0702 (Linking)
VI  - 142
IP  - 1-2
DP  - 2008 Nov 3
TI  - Specific inflammatory condition in nucleus tractus solitarii of the SHR: novel 
      insight for neurogenic hypertension?
PG  - 25-31
LID - 10.1016/j.autneu.2008.07.003 [doi]
AB  - Human essential hypertension is a complex polygenic trait with underlying genetic 
      components that remain unknown. Since the brainstem structure--the nucleus of the 
      solitary tract (NTS)--is a pivotal region for regulating the set-point of 
      arterial pressure, we proposed a role for it in the development of primary 
      hypertension. Using microarray and real-time RT-PCR, we have recently identified 
      that some pro-inflammatory molecules, such as junctional adhesion molecule-1 
      (JAM-1; a leukocyte/platelet adhesion molecule), were over expressed in 
      endothelial cells in the NTS of an animal model of human essential 
      hypertension--the spontaneously hypertensive rat (SHR) compared to normotensive 
      Wistar Kyoto rats (WKY). Adenoviral mediated over expression of JAM-1 in NTS of 
      WKY rats produced both hypertension and localized leukocyte adherence to the 
      microvasculature. With a known effect of leukocyte adhesion causing cytokine 
      release, we predicted differences in the level of gene expression of cytokines in 
      the NTS of SHR relative to WKY. Gene expression of monocyte chemoattractant 
      protein-1 (MCP-1) was higher in the NTS of SHR while inter-leukin-6 (IL-6) was 
      lower in the NTS of SHR compared to the WKY. Because both inflammatory molecules 
      are known to affect neural functions, our data suggest that the microvasculature 
      of NTS of the SHR exhibits a specific inflammatory state. We propose a new 
      hypothesis that as a consequence of enhanced expression of leukocyte adhesion 
      molecules within the microvasculature of NTS there is a specific inflammatory 
      response that leads to cardiovascular autonomic dysfunction contributing to 
      neurogenic hypertension.
FAU - Waki, Hidefumi
AU  - Waki H
AD  - Department of Physiology, Wakayama Medical University School of Medicine, 811-1, 
      Kimiidera, Wakayama 641-8509, Japan. h-waki@wakayama-med.ac.jp
FAU - Gouraud, Sabine S
AU  - Gouraud SS
FAU - Maeda, Masanobu
AU  - Maeda M
FAU - Paton, Julian F R
AU  - Paton JF
LA  - eng
GR  - RG/07/006/23634/BHF_/British Heart Foundation/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20080821
PL  - Netherlands
TA  - Auton Neurosci
JT  - Autonomic neuroscience : basic & clinical
JID - 100909359
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (F11r protein, rat)
RN  - 0 (Interleukin-6)
SB  - IM
MH  - Animals
MH  - Cell Adhesion/genetics/immunology
MH  - Cell Adhesion Molecules/genetics/metabolism
MH  - Chemokine CCL2/genetics
MH  - Chemotaxis, Leukocyte/genetics
MH  - Disease Models, Animal
MH  - Encephalitis/*immunology
MH  - Humans
MH  - Hypertension/*immunology
MH  - Interleukin-6/genetics
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Solitary Nucleus/*immunology
RF  - 66
EDAT- 2008/08/30 09:00
MHDA- 2009/01/23 09:00
CRDT- 2008/08/30 09:00
PHST- 2008/02/14 00:00 [received]
PHST- 2008/06/24 00:00 [revised]
PHST- 2008/07/01 00:00 [accepted]
PHST- 2008/08/30 09:00 [pubmed]
PHST- 2009/01/23 09:00 [medline]
PHST- 2008/08/30 09:00 [entrez]
AID - S1566-0702(08)00125-2 [pii]
AID - 10.1016/j.autneu.2008.07.003 [doi]
PST - ppublish
SO  - Auton Neurosci. 2008 Nov 3;142(1-2):25-31. doi: 10.1016/j.autneu.2008.07.003. 
      Epub 2008 Aug 21.