| Summary: | 碩士 === 國立臺灣大學 === 動物學研究所 === 96 === Voltage-gated T-type Ca2+ current (T-current) is temporarily recorded in cardiac myocytes during embryonic and postnatal period in some rodents (Leuranguer et al., 2000; Niwa et al., 2004) and was found linearly correlated with growth rate in rat of both sexes (Xu and Best, 1992). The growth of body weight and heart size has been well studied to be affected by chronically elevated growth hormone (GH) through the action of Insulin-like growth factor-1 (IGF-1) (Boguszewski et al., 1997; Ong et al., 2002; Xu and Best, 1991). Moreover, through the approach of patch-clamp, IGF-1 was found to be able to increase the current density of T-channels (Piedras-Renteria et al., 1997). Collectively, physiological cardiac hypertrophy in athletes is associated with increased cardiac IGF-1 formation, implying that T-channel might play a role in the physiological cardiac hypertrophy formation. To test the hypothesis that T-channels are involved in that cardiac remodeling during physiological cardiac hypertrophy, CaV3.2 T-type calcium channel deficient mice (CaV3.2-/-) were subjected to swimming training for 3 weeks and the development of cardiac hypertrophy was examined with echocardiography. At the basal level, there is no significant difference between wild type (WT) and CaV3.2-/- left ventricular mass (LVM) but after 3 weeks of swimming, WT showed a significant increase of LVM (0.11 ±0.0028 g (WT non-swim, n=7) and 0.13 ± 0.0029 g (WT swim, n=7, p<0.001). In contrast, swimming-induced physiological cardiac hypertrophy was blunted in CaV3.2-/-, the LVM were 0.1099 ± 0.005 (CaV3.2-/- non-swim, n=5) and 0.1036 ± 0.0028 (CaV3.2-/- swim 21ds, n=5, p=0.3). These findings suggest that CaV3.2 is necessary for triggering swimming-induced physiological cardiac hypertrophy.
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