The Japanese Journal of Physiology
Print ISSN : 0021-521X
52 巻, 6 号
選択された号の論文の9件中1~9を表示しています
Regular Papers
  • Wei Wang, Naoki Hino, Hiroshi Yamasaki, Takashi Aoki, Rikuo Ochi
    2002 年 52 巻 6 号 p. 507-514
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    The H9c2 clonal cell line derived from embryonic rat ventricle is an in vitro model system for cardiac and skeletal myocytes. We used the whole-cell patch clamp technique to characterize the electrophysiological and pharmacological properties of an outward K+ current (IKV) and determined its molecular correlate in H9c2 myoblasts. IKV was activated by threshold depolarization to −30 mV, and its current amplitude and rate of activation increased with further depolarizations. IKV inactivated slowly with a time constant of 1–2 s, and the V0.5 for steady-state inactivation was −37.9 ± 4.6 mV (n = 10). Tetraethylammonium and quinidine suppressed IKV with IC50's of 3.7 mM and 11.6 μM, respectively. Using RT-PCR analysis we found that the KV 2.1 gene is the most abundantly expressed among genes for KV1.2, 1.4, 1.5, 2.1, 4.2, and 4.3, and by Western blotting we confirmed the synthesis of the KV2.1 α-subunit protein. We conclude that IKV, the predominant voltage-gated outward current in H9c2 myoblasts, flows through the channels comprised of the KV2.1-subunit gene product.
  • Eiko Inagaki, Koichi Kawamata, Yuichi Suzuki
    2002 年 52 巻 6 号 p. 515-520
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    Ingested K+ is believed to be absorbed mainly in the small intestine by passive diffusion through the paracellular pathway. To further clarify K+ absorption in the small intestine, we determined the unidirectional flux values of Rb+ in vitro by atomic absorption spectroscopy in the mouse ileum mounted in Ussing chambers under short-circuit conditions. The mucosal-to-serosal Rb+ flux (Jms) was larger than the serosal-to-mucosal Rb+ flux (Jsm), resulting in positive net Rb+ absorption (Jnet). The effect of changing the transmucosal potential (Vt) showed that Jms was composed of both a Vt-dependent diffusion component and a Vt-independent non-diffusion component, while Jsm was composed mainly of a Vt-dependent component. A forskolin treatment eliminated Jnet mainly due to the increase in Jsm. When animals were fed a low-Na diet, Jnet was mainly eliminated as a result of the increase in Jsm. These findings suggest that K+ is absorbed not only by passive diffusion through the paracellular pathway, but also by an active transport mechanism operating through the cellular pathway. In addition, cAMP and aldosterone may be involved in regulating intestinal K+ transport.
  • Tomoko Koeda, Jun Sato, Takao Kumazawa, Yoichiro Tsujii, Kazue Mizumur ...
    2002 年 52 巻 6 号 p. 521-530
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    There is some evidence that the sympathetic nervous system plays a role in the development and/or maintenance of painful states, and that sympathetic nervous function is altered in these conditions. Our previous experiments showed that electrical stimulation of the lumbar sympathetic trunk (sympathetic stimulation: SS), which normally induces a decrease in blood flow (BF) of plantar skin, induced its BF increase in about 50% of adjuvant-inflamed rats. To investigate the mechanism of this BF-increase response, we examined whether noradrenaline (NA) plays any role in this changed response to SS, and which receptor subtype is involved. We measured paw cutaneous BF response with a laser Doppler flowmeter in rats chronically inflamed with complete Freund's adjuvant. SS induced the BF-increase response in 50–67% of measured sites. Close-arterially injected NA induced the BF-increase response at dosages between 10–100 ng/kg only at the sites with the BF-increase response to SS. The BF-increase and -decrease responses to NA was significantly reduced after the close-arterial injection of either α1- or α2-adrenoceptor antagonists (p lt; 0.05, respectively). In contrast, although the BF-decrease responses to SS were significantly reduced by administration of α1- and α2-adrenoceptor antagonist, BF-increase response was reduced only by α1-adrenoceptor antagonist, and that only at a higher dose. In addition, the β-adrenoceptor antagonist had no effects on both responses. These results suggest that the BF-increase response to SS involves, additionally to NA, a non-adrenergic mechanism.
  • Yoichiro Kusakari, Kenichi Hongo, Makoto Kawai, Masato Konishi, Satosh ...
    2002 年 52 巻 6 号 p. 531-539
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    We investigated the mechanism of α1-adrenoceptor stimulation on the myofibrillar Ca2+ responsiveness at steady-state in intact rat ventricular myocytes. We produced tetanus, and an instantaneous plot of [Ca2+]i vs. cell length (Ca–L trajectory) was constructed to estimate the Ca2+ responsiveness. An α1-agonist, phenylephrine, dose-dependently shifted the Ca–L trajectory to the left, corresponding to sensitization of the myofilaments. An α1-antagonist, prazosin, and inhibition of the Na/H exchange by ethylisopropylamiloride (EIPA) completely reversed the phenylephrine-induced shift. Phenylephrine increased pHi (ΔpHi = +0.1), which was reversed by prazosin and EIPA. Chelerythrine, an inhibitor of protein kinase C (PKC), completely blocked the effects of phenylephrine on Ca2+ responsiveness and pHi. When pHi was increased (ΔpHi = +0.1) without phenylephrine by changing pHo, the Ca–L trajectory was shifted to the same extent as that observed with phenylephrine. We conclude that α1-adrenoceptor stimulation activates Na/H exchange through a PKC-mediated pathway and that an increase in pHi is mainly responsible for the increase in Ca2+ responsiveness.
  • Michiko Tashiro, Pulat Tursun, Takefumi Miyazaki, Masaru Watanabe, Mas ...
    2002 年 52 巻 6 号 p. 541-551
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    To study Mg2+ transport across the cell membrane, the cytoplasmic concentration of Mg2+ ([Mg2+]i) in rat ventricular myocytes was measured with the fluorescent indicator furaptra (mag-fura-2) under Ca2+-free conditions (0.1 mM EGTA) at 25°C. The fluorescence ratio signal of furaptra was converted to [Mg2+]i using calibration parameters previously estimated in myocytes (Watanabe and Konishi, Pflügers Arch 442: 35–40, 2001). After [Mg2+]i was raised by loading the cells with Mg2+ in a solution containing 93 mM Mg2+, the cells were voltage-clamped at a holding potential of −80 mV using the perforated patch–clamp technique with amphotericin B. At the holding potential of −80 mV, the reduction of extracellular Mg2+ to 1.0 mM caused a rapid decrease in [Mg2+]i only in the presence of extracellular Na+. The rate of the net Mg2+ efflux appeared to be dependent on the initial level of [Mg2+]i; the decrease in [Mg2+]i was significantly faster in the myocytes markedly loaded with Mg2+. The rate of decrease in [Mg2+]i was influenced little by membrane depolarization from −80 to −40 mV, but the [Mg2+]i decrease accelerated significantly at 0 mV by, on average, ∼40%. Hyperpolarization from −80 to −120 mV slightly but significantly slowed the decrease in [Mg2+]i by ∼20%. The results clearly demonstrate an extracellular Na+- and intracellular Mg2+-dependent Mg2+ efflux activity, which is consistent with the Na+–Mg2+ exchange, in rat ventricular myocytes. We found that the apparent rate of Mg2+ transport depends slightly on the membrane potential: facilitation by depolarization and inhibition by hyperpolarization with no sign of reversal between −120 and 0 mV.
  • Kazuko Takase, Takeshi Nishiyasu, Katsumi Asano
    2002 年 52 巻 6 号 p. 553-560
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    The purpose of this study was to examine the hypothesis that the menstrual cycle–induced modulation of the cardiorespiratory response to exercise might be altered by acute exposure to altitude. During both the luteal and follicular phases, 9 moderately trained female subjects with normal menstrual cycles performed incremental exercise to maximal effort on a cycle ergometer at sea level (SL) and under hypobaric hypoxia (HH) at the equivalent of 3,000 m altitude. Both at rest and during exercise, minute ventilation (V˙E) and oxygen uptake (V˙O2) did not differ between the luteal and follicular phases (either at SL or HH). However, the ratio of V˙E to V˙O2 (V˙E/V˙O2), both at rest and during peak exercise, was greater in the luteal phase than in the follicular phase under HH conditions. Furthermore, the partial pressure of end-tidal carbon dioxide (PETCO2) during exercise was lower in the luteal phase than in the follicular phase in HH. These results suggest that the menstrual cycle–induced modulation of the ventilatory response to exercise may be altered under acute hypobaric-hypoxic conditions.
  • Keita Hosoi, Kyong-Yob Minp, Chisa Shiima, Toshiaki Hanafusa, Hiroshi ...
    2002 年 52 巻 6 号 p. 561-572
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    Changes in the volume of rat alveolar type II cells (AT-II cells) induced by terbutaline, a β2-agonist, were measured using video-enhanced contrast microscopy. The changes consisted of three phases: initial cell shrinkage, cell swelling, and gradual cell shrinkage. The initial cell shrinkage was Ca2+-dependent and was inhibited by quinine (a K+ channel blocker). The subsequent cell swelling was cAMP-dependent and was inhibited by amiloride (a Na+ channel blocker). The final cell shrinkage was cAMP-dependent and was inhibited by 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB, a Cl channel blocker). Thus, terbutaline-induced cell volume changes were regulated by both Ca2+ and cAMP. Accumulation of cAMP alone, however, induced the Ca2+-dependent cell shrinkage of AT-II cells and H-89 (a PKA inhibitor) inhibited terbutaline-induced cell volume changes. This suggests that cAMP accumulation stimulates the Ca2+ signal during terbutaline stimulation. In conclusion, terbutaline stimulates not only Na+ influx, but also K+ and Cl release mediated via cAMP accumulation in rat AT-II cells, which induces the triphasic cell volume changes.
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