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KMID : 0811720090130030153
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Korean Journal of Physiology & Pharmacology
2009 Volume.13 No. 3 p.153 ~ p.159
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Deficiency of iNOS Does Not Prevent Isoproterenol-induced Cardiac Hypertrophy in Mice
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Cha Hye-Na
Hong Geu-Ru
Kim Yong-Woon
Kim Jong-Yeon
Dan Jin-Myoung
Park So-Young
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Abstract
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We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-? (TGF-?) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-? (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-? in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol- induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.
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KEYWORD
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Inducible nitric oxide synthase, Isoproterenol, Cardiac hypertrophy
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