Abstract | AIM: METHODS AND RESULTS: In human fibroblasts 1-butanol inhibited collagen synthesis and enhanced collagenase production, but iso- butanol did not. These indicate crucial roles of PLD in collagen synthesis and degradation. In fibroblasts, MEA dose-dependently decreased PLD activity, inhibited collagen synthesis and enhanced collagenase production. In a hypertensive heart failure model using Dahl-Iwai salt-sensitive rats, PLD activity increased with progressive ventricular fibrosis, leading to myocardial stiffening and overt heart failure. Long-term administration of MEA did not significantly decrease blood pressure, however, but decreased PLD activity and collagen content with inhibited gene expression of collagens, leading to the prevention of myocardial stiffening and haemodynamic deterioration. MEA also attenuated ventricular hypertrophy, another detrimental structural alteration. CONCLUSION:
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Authors | Kazuhiro Yamamoto, Yoshito Takahashi, Toshiaki Mano, Yasushi Sakata, Nagahiro Nishikawa, Junichi Yoshida, Yuichi Oishi, Masatsugu Hori, Takeshi Miwa, Shintaro Inoue, Tohru Masuyama |
Journal | European heart journal
(Eur Heart J)
Vol. 25
Issue 14
Pg. 1221-9
(Jul 2004)
ISSN: 0195-668X [Print] England |
PMID | 15246640
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Enzyme Inhibitors
- Ethanolamines
- Collagen
- Phospholipase D
- Collagenases
- N-methylaminoethanol
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Topics |
- Animals
- Blood Pressure
(physiology)
- Collagen
(antagonists & inhibitors)
- Collagenases
(drug effects, metabolism)
- Enzyme Inhibitors
(pharmacology, therapeutic use)
- Ethanolamines
(pharmacology, therapeutic use)
- Fibroblasts
(drug effects, metabolism)
- Fibrosis
(enzymology, prevention & control)
- Heart Ventricles
(enzymology, pathology)
- Male
- Phospholipase D
(antagonists & inhibitors, drug effects)
- Rats
- Rats, Inbred Dahl
- Ventricular Dysfunction
(enzymology, prevention & control)
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