PMID- 9476582
OWN - NLM
STAT- MEDLINE
DCOM- 19980407
LR  - 20211203
IS  - 0910-8327 (Print)
IS  - 0910-8327 (Linking)
VI  - Suppl 12
DP  - 1997
TI  - Role of cardiac nonmyocytes in cyclic mechanical stretch-induced myocyte 
      hypertrophy.
PG  - 198-200
AB  - In cardiac hypertrophy or ventricular remodeling, not only the enlargement of 
      myocytes but also interstitial or perivascular fibrosis are observed 
      simultaneously, which suggests an interaction between cardiac myocytes and 
      fibroblasts. In this study, we examined the mechanism of cyclic mechanical 
      stretch-induced myocyte hypertrophy, highlighting the interaction between 
      myocytes and cardiac nonmyocytes, mostly fibroblasts. Ventricular myocytes (MC) 
      and cardiac nonmyocytes (NMC) were separately extracted from neonatal rat 
      ventricles by the discontinuous Percoll gradient method and primary cultures of 
      cardiac cells were prepared. Cyclic mechanical stretch was applied to the 
      cultures with a Flexercell Stress Unit. In addition to cell size, we examined 
      atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP) production as the 
      most sensitive biological markers for MC hypertrophy. Cyclic stretch did not 
      induce hypertrophic responses in MC when they were cultured without NMC. In 
      contrast, when MC were co-cultured with NMC, cyclic stretch induced further 
      increase in ANP/BNP production (2.2-fold and 2.1-fold increases versus 
      non-stretch group, after 48-h incubation). This increase in ANP/BNP production in 
      the co-culture was significantly suppressed by CV-11974, an angiotensin II type 1 
      receptor antagonist. Moreover, ANP/BNP production in the co-culture was 
      significantly suppressed by BQ-123, an endothelin A receptor antagonist, whether 
      cyclic stretch was applied or not. This study raised the possibility that NMC 
      mediate the hypertrophic effect of mechanical stress on MC by increasing 
      endothelin production. It was also suggested that, in this process, angiotensin 
      II is involved in the crosstalk between MC and NMC.
FAU - Harada, M
AU  - Harada M
AD  - Department of Medicine and Clinical Science, Kyoto University Graduate School of 
      Medicine, Japan.
FAU - Saito, Y
AU  - Saito Y
FAU - Nakagawa, O
AU  - Nakagawa O
FAU - Miyamoto, Y
AU  - Miyamoto Y
FAU - Ishikawa, M
AU  - Ishikawa M
FAU - Kuwahara, K
AU  - Kuwahara K
FAU - Ogawa, E
AU  - Ogawa E
FAU - Nakayama, M
AU  - Nakayama M
FAU - Kamitani, S
AU  - Kamitani S
FAU - Hamanaka, I
AU  - Hamanaka I
FAU - Kajiyama, N
AU  - Kajiyama N
FAU - Masuda, I
AU  - Masuda I
FAU - Itoh, H
AU  - Itoh H
FAU - Tanaka, I
AU  - Tanaka I
FAU - Nakao, K
AU  - Nakao K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Heart Vessels
JT  - Heart and vessels
JID - 8511258
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Benzimidazoles)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Endothelin Receptor Antagonists)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (Tetrazoles)
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))
RN  - S8Q36MD2XX (candesartan)
SB  - IM
MH  - Angiotensin Receptor Antagonists
MH  - Animals
MH  - Atrial Natriuretic Factor/analysis
MH  - Benzimidazoles/pharmacology
MH  - Biphenyl Compounds
MH  - Cardiomegaly/pathology/*physiopathology
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Endothelin Receptor Antagonists
MH  - Fibroblasts/*pathology
MH  - Myocardium/cytology/*pathology
MH  - Natriuretic Peptide, Brain
MH  - Nerve Tissue Proteins/analysis
MH  - Peptides, Cyclic/antagonists & inhibitors
MH  - Rats
MH  - Stress, Mechanical
MH  - Tetrazoles/pharmacology
EDAT- 1997/01/01 00:00
MHDA- 1998/02/26 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1998/02/26 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
PST - ppublish
SO  - Heart Vessels. 1997;Suppl 12:198-200.