PMID- 16231753
OWN - NLM
STAT- MEDLINE
DCOM- 20051110
LR  - 20061115
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 28
IP  - 6
DP  - 2005 Jun
TI  - Diastolic dysfunction in hypertensive hearts: roles of perivascular inflammation 
      and reactive myocardial fibrosis.
PG  - 483-90
AB  - There is increasing evidence that myocardial fibrosis plays a role in the 
      pathogenesis of diastolic dysfunction in hypertensive heart disease. However, it 
      has been difficult to explore the mechanisms of isolated diastolic dysfunction in 
      hypertensive hearts because of the lack of adequate animal models. Recently, we 
      demonstrated that Wistar rats with a suprarenal aortic constriction (AC) can be 
      used as a model of cardiac hypertrophy associated with preserved systolic, but 
      impaired diastolic function without overt congestive heart failure. In this 
      model, acute pressure elevation induces reactive myocardial fibrosis 
      (perivascular fibrosis followed by intermuscular interstitial fibrosis) and 
      myocyte/left ventricular (LV) hypertrophy. Perivascular macrophage infiltration, 
      which is mediated by monocyte chemoattractant protein-1 (MCP-1) and intercellular 
      adhesion molecule-1, exerts a key role in myocardial fibrosis, but not in 
      myocyte/LV hypertrophy. Transforming growth factor (TGF)-beta is crucial for 
      reactive fibrosis in AC rats. MCP-1 function blocking not only inhibits 
      macrophage infiltration and TGF-beta induction but also prevents reactive 
      fibrosis and diastolic dysfunction, without affecting blood pressure, myocyte/LV 
      hypertrophy, or systolic function. Accordingly, a substantial role of 
      inflammation is indicated in myocardial fibrosis and diastolic dysfunction in 
      hypertensive hearts. Currently, the precise mechanisms whereby acute pressure 
      elevation triggers inflammation remain unknown, but it is likely that activation 
      of the tissue angiotensin system is involved in the induction of the inflammatory 
      process.
FAU - Kai, Hisashi
AU  - Kai H
AD  - Third Department of Internal Medicine and Cardiovascular Research Institute, 
      Kurume University School of Medicine, Kurume, Japan. naikai@med.kurume-u.ac.jp
FAU - Kuwahara, Fumitaka
AU  - Kuwahara F
FAU - Tokuda, Keisuke
AU  - Tokuda K
FAU - Imaizumi, Tsutomu
AU  - Imaizumi T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
SB  - IM
MH  - Animals
MH  - Coronary Circulation/*physiology
MH  - Diastole/*physiology
MH  - Fibrosis
MH  - Humans
MH  - Myocardium/pathology
MH  - Vasculitis/immunology/pathology/*physiopathology
MH  - Ventricular Dysfunction, Left/immunology/pathology/*physiopathology
RF  - 53
EDAT- 2005/10/20 09:00
MHDA- 2005/11/11 09:00
CRDT- 2005/10/20 09:00
PHST- 2005/10/20 09:00 [pubmed]
PHST- 2005/11/11 09:00 [medline]
PHST- 2005/10/20 09:00 [entrez]
AID - 10.1291/hypres.28.483 [doi]
PST - ppublish
SO  - Hypertens Res. 2005 Jun;28(6):483-90. doi: 10.1291/hypres.28.483.