Abstract | OBJECTIVES: BACKGROUND: Chronic inhibition of nitric oxide (NO) synthesis induces cardiac hypertrophy independent of blood pressure by increasing protein synthesis in vivo. KCOs attenuate calcium overload and confer cardioprotection against ischemic stress, and thereby prevent myocardial remodeling. METHODS: RESULTS:
L-NAME increased blood pressure and LVW/BW compared with the control. KCOs and hydralazine equally cancelled the increase in blood pressure, whereas only KCOs blocked the increase in LVW/BW and myocardial hypertrophy induced by L-NAME. The L-NAME group showed both p70S6K and ERK activation in the myocardium compared with the control(2.3-fold and 2.0-fold, respectively), which was not reversed by hydralazine. Selective inhibition of either P70S6K or ERK blocked myocardial hypertrophy. KCOs prevented the increase in activity only of p70S6K. Glibenclamide reversed the effect of nicorandil in the presence of L-NAME. CONCLUSIONS:
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Authors | Shoji Sanada, Koichi Node, Hiroshi Asanuma, Hisakazu Ogita, Seiji Takashima, Tetsuo Minamino, Masanori Asakura, Masatsugu Hori, Masafumi Kitakaze |
Journal | Journal of cardiology
(J Cardiol)
Vol. 41
Issue 1
Pg. 43-4
(Jan 2003)
ISSN: 0914-5087 [Print] Netherlands |
PMID | 12564115
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- Chromans
- JTV 506
- Potassium Channels
- Hydralazine
- Nitric Oxide
- Adenosine Triphosphate
- Ribosomal Protein S6 Kinases, 70-kDa
- Mitogen-Activated Protein Kinases
- NG-Nitroarginine Methyl Ester
- Sirolimus
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Topics |
- Adenosine Triphosphate
(physiology)
- Animals
- Blood Pressure
(drug effects)
- Cardiomegaly
(etiology)
- Chromans
(pharmacology)
- Hydralazine
(pharmacology)
- Mitogen-Activated Protein Kinases
(physiology)
- NG-Nitroarginine Methyl Ester
(pharmacology)
- Nitric Oxide
(biosynthesis, blood)
- Potassium Channels
(physiology)
- Rats
- Rats, Inbred WKY
- Ribosomal Protein S6 Kinases, 70-kDa
(physiology)
- Sirolimus
(pharmacology)
- Ventricular Remodeling
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