| Autor: |
Tsai-Wen Wu, Kyoichi Ono, Murakami, Manabu, Iijima, Toshihiko |
| Předmět: |
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| Zdroj: |
Pharmacology; 2006, Vol. 76 Issue 4, p170-179, 10p, 4 Graphs |
| Abstrakt: |
Noradrenaline release from sympathetic nerve terminals is dependent on Ca2+ entry through neuronal voltage-gated N-type Ca2+ channels. The accessory β3 subunits of Ca2+ channels (CaVβ3) are preferentially associated with the α1B subunit to form N-type Ca2+ channels, and are therefore expected to play a functional role in the stimulation-evoked release of noradrenaline. In this study, we employed CaVβ3-null, CaVβ3-overexpressing (CaVβ3-Tg), and wild-type (WT) mice to investigate the possible roles of CaVβ3 in the sympathetic regulation of heart rate in vivo. Telemetry was used to monitor the ECG and both time and frequency domain analyses were carried out to evaluate heart rate variability. In the frequency domain analysis, power spectral density of the RR interval series was computed using the fast Fourier transform algorithm. The resting heart rate was increased in CaVβ3-Tg mice compared with both CaVβ3-null and WT mice. Mice overexpressing CaVβ3 displayed decreased heart rate variability, which was measured by the time domain analysis of the standard deviation of RR intervals. In the frequency domain analysis, CaVβ3-Tg mice showed decreased spectral powers compared with WT and CaVβ3-null mice. Pharmacological blockade of β-adrenergic receptors with metoprolol decreased the heart rate in all genotypes, but the extent of the decrease was most obvious in CaVβ3-Tg mice. On the other hand, the spectral powers were decreased in response to parasympathetic blockade (atropine) in WT and CaVβ3-Tg mice. These results indicate the functional roles of CaVβ3 in regulating sympathetic nerve signaling. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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