PMID- 15076165
OWN - NLM
STAT- MEDLINE
DCOM- 20041018
LR  - 20190823
IS  - 0263-6352 (Print)
IS  - 0263-6352 (Linking)
VI  - 22
IP  - 3
DP  - 2004 Mar
TI  - Eprosartan improves cardiac performance, reduces cardiac hypertrophy and 
      mortality and downregulates myocardial monocyte chemoattractant protein-1 and 
      inflammation in hypertensive heart disease.
PG  - 583-92
AB  - OBJECTIVE: The purpose of this investigation was to determine whether angiotensin 
      II receptor (AII1R) antagonism interferes with cardiac monocyte chemoattractant 
      protein-1 (MCP-1) expression in hypertrophic cardiomyopathy and failure. DESIGN: 
      We studied the effects of the AII1R antagonist eprosartan on MCP-1 expression, 
      and on the recruitment of macrophages into the myocardium in a model of cardiac 
      hypertrophy and morbidity/mortality. METHODS: Stroke-prone spontaneously 
      hypertensive rats fed a high-salt, high-fat diet (SFD) developed heart failure 
      characterized by left ventricular (LV) hypertrophy/pathology and 
      hypocontractility. These rats received either normal diet, SFD, or SFD with the 
      daily administration of 30 mg/kg eprosartan for 28 weeks. LV function and wall 
      thickness was assessed by echocardiography, MCP-1 expression was measured by 
      TaqMan real-time polymerase chain reaction, enzyme-linked immunosorbent assay and 
      immunohistochemistry, and macrophage infiltration into the LV was determined by 
      microscopy. RESULTS: Eprosartan reduced the rate of morbidity/mortality (P = 
      0.001), LV MCP-1 mRNA (P < 0.05) and protein expression (P < 0.01), and LV 
      macrophage infiltration (P < 0.01), while preserving ventricular function (P < 
      0.05). Eprosartan also produced a moderate (16%; P < 0.05) decrease in blood 
      pressure. CONCLUSIONS: These data demonstrate that AII1R antagonism in an animal 
      model of hypertensive heart disease reduces MCP-1 expression in the myocardium 
      that results in reduced macrophage recruitment. These effects parallel the 
      preservation of LV systolic function and the reduction in cardiac 
      remodeling/disease progression and reduced morbidity/mortality. Suppression of 
      MCP-1 expression might explain in part the beneficial effects of AII1R antagonism 
      in this model.
FAU - Behr, Thomas M
AU  - Behr TM
AD  - Medizinische Poliklinik, Department of Cardiology, University of Wuerzburg, 
      Germany. t.behr@medizin.uni-wuerzburg.de
FAU - Willette, Robert N
AU  - Willette RN
FAU - Coatney, Robert W
AU  - Coatney RW
FAU - Berova, Marinela
AU  - Berova M
FAU - Angermann, Christiane E
AU  - Angermann CE
FAU - Anderson, Karen
AU  - Anderson K
FAU - Sackner-Bernstein, Jonathan D
AU  - Sackner-Bernstein JD
FAU - Barone, Frank C
AU  - Barone FC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 0 (Acrylates)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Imidazoles)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiophenes)
RN  - 11128-99-7 (Angiotensin II)
RN  - 2KH13Z0S0Y (eprosartan)
SB  - IM
CIN - J Hypertens. 2004 Mar;22(3):451-4. PMID: 15076146
MH  - Acrylates/*administration & dosage
MH  - Angiotensin II/antagonists & inhibitors
MH  - Animals
MH  - Antihypertensive Agents/*administration & dosage
MH  - Chemokine CCL2/*genetics/metabolism
MH  - Down-Regulation/drug effects
MH  - Hypertension/*drug therapy/immunology/mortality
MH  - Hypertrophy, Left Ventricular/diagnostic imaging/*drug therapy/mortality
MH  - Imidazoles/*administration & dosage
MH  - Immunohistochemistry
MH  - Macrophages/cytology/immunology/metabolism
MH  - Myocardial Contraction/drug effects
MH  - Myocardium/immunology/metabolism
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Inbred SHR
MH  - *Thiophenes
MH  - Ultrasonography
MH  - Vasculitis/diagnostic imaging/drug therapy/mortality
EDAT- 2004/04/13 05:00
MHDA- 2004/10/19 09:00
CRDT- 2004/04/13 05:00
PHST- 2004/04/13 05:00 [pubmed]
PHST- 2004/10/19 09:00 [medline]
PHST- 2004/04/13 05:00 [entrez]
AID - 00004872-200403000-00022 [pii]
AID - 10.1097/00004872-200403000-00022 [doi]
PST - ppublish
SO  - J Hypertens. 2004 Mar;22(3):583-92. doi: 10.1097/00004872-200403000-00022.