The Japanese Journal of Physiology
Print ISSN : 0021-521X
52 巻, 3 号
選択された号の論文の11件中1~11を表示しています
Regular Papers
  • Motoko Ohira, Hagino Hanada, Fuminori Kawano, Akihiko Ishihara, Ikuya ...
    2002 年 52 巻 3 号 p. 235-245
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    The mechanisms responsible for the morphological and metabolic adaptation of skeletal muscles to the removal of antigravity activity were investigated in rats. Significant atrophy relative to the levels before suspension was induced in ankle plantarflexsors, may be due to a reduced tension production caused by decreased muscle length and electromyogram activity. Growth failure was significant in ankle dorsiflexors, although these muscles did not atrophy. Forced muscle contraction through electrical stimulation at 1 or 100 Hz during hind limb suspension generally had detrimental effects. The percent contribution of water loss to the suspension-related change in weight was 85, 88, and 93% in soleus, plantaris, and extensor digitorum longus, respectively. The total levels of both β-hydroxyacyl CoA dehydrogenase (HAD) and lactate dehydrogenase (LDH) were less in the suspended muscles than in the controls, having high positive correlations with the total protein content. The specific activity of HAD, but not of LDH, of the suspended muscles was lower than in the controls (25–61%). These data suggest that the cause of muscle atrophy and changes in metabolic properties may be a decreased tension development, not necessarily the reduction of electrical or contractile activity. Further, it is clearly suggested that electrical stimulation of a muscle group with different composition of fiber phenotype at a certain pattern or frequency is not suitable for the countermeasure. It is also suggested that the major cause of the decreased muscle weight was loss of water, even though protein content was also lowered after suspension. Moreover, the data suggest that the HAD level was affected more than the total protein content and LDH.
  • Haruka Murakami, Akemi Ota, Hitoshi Simojo, Morihiko Okada, Ryuichi Aj ...
    2002 年 52 巻 3 号 p. 247-256
    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 investigate whether the polymorphisms in the control region of mitochondrial DNA (mtDNA) related to individual difference in the endurance capacity or trainability. Fifty-five sedentary males participated in this study and were submitted to an 8-week endurance training program. The VO2 max was determined before and after training. Total DNA was extracted from the blood, and the sequence of the mtDNA control region was determined. The polymorphism in the mtDNA control region was decided based on the "Cambridge sequence." In 29 of the 55 subjects, vastus lateralis muscle biopsy samples were taken at rest before and after the training program. MtDNA content and CS (citrate synthase) activity in skeletal muscle was measured as the phenotype of the polymorphisms in the mtDNA control region. The VO2 max increased to 48.2 ± 6.3 ml/min/kg from 42.1 ± 6.0 as a result of the 8-week training (p < 0.05). The numbers of polymorphisms in determined 1,122 bp were 11.1 ± 2.9 variable sites per person, and the total numbers of polymorphisms were 125 variable sites. The subjects were classified into two groups at each variable site, the Cambridge sequence (Cam) group and the non-Cambridge sequence (non-Cam) group. There were significant differences in pre-VO2 max between the two groups at each mtDNA nucleotide positions 16298, 16325, and 199, and in %ΔVO2 max at 16223 and 16362. Twenty-nine subjects who underwent the biopsy revealed significant differences in pre-CS activity at 194 and pre-mtDNA content at 514. Also, significant differences were found in the change rate of VO2 max and CS activity as a result of training between the two groups at 16519. In conclusion, it suggested that mtDNA polymorphisms in the control region might result in individual differences in endurance capacity or trainability.
  • Shinjiro Yamaguchi, Momoyo Ito, Norio Ohshima
    2002 年 52 巻 3 号 p. 257-265
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    The effects of electrical stimulation of the dorsal skin area on the mesenteric arterioles were investigated in anesthetized rats by the use of an intravital microscope-television system. Changes in the diameter of the mesenteric precapillary arterioles (10–40 μm in diameter) were measured with an image processor. Blood flow velocity in the mesenteric precapillary arterioles was monitored by the dual sensor method developed by the authors. Electrical stimulation was performed through two platinum electrodes placed at the right dorsal Th5-12 level skin area by the use of an electrical stimulator (0.2 ms, 20 Hz). Continuous stimulation lasting for 30 s (1–10 mA) and intermittent stimulation lasting for 10 min (3 mA) were applied. The pressor response following the depressor response was induced by a stimulus current above 8 mA. The decrease in mesenteric blood flow velocity was induced by stimulus current above 10 mA. These responses were abolished by lidocaine injection into the subcutaneous area where the electrodes were attached. No significant change in arteriolar diameter or heart rate were induced by the stimulation for 30 s. Electrical stimulation of the skin for 10 min evoked a decrease in the diameter of arterioles (−3.4 ± 2%, p < 0.01, n = 12). In the adrenalectomized group, electrical stimulation of the skin for 10 min elicited a slight increase in the diameter (1.1 ± 0.5%, n = 6). It is therefore suggested that electrical stimulation of the skin for 30 s reflexly evoked decreases in MAP and in blood flow velocity, and that the constriction of the mesenteric precapillary arterioles induced by the stimulation for 10 min was mediated by humoral adrenaline and noradrenaline released by somato-adrenal medullary reflex.
  • Junko Hirano, Kazuyoshi Nakamura, Shun-ichi Itazawa, Yoshiro Sohma, Ta ...
    2002 年 52 巻 3 号 p. 267-276
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    The Ca2+-activated and voltage-sensitive large conductance K+ channel (BK channel) with a slope conductance of about 300 pS is present in the surface membrane of cultured human renal proximal tubule epithelial cells (RPTECs). In this study we examined the effects of cytoplasmic pH (pHi) on activity and gating kinetics of the BK channel by using the inside-out configuration of the patch-clamp technique. At a constant cytoplasmic Ca2+ concentration ([Ca2+]i), membrane depolarization raised channel open probability (Po), and lowering pHi shifted the Po–membrane potential (Vm) relationship to the positive voltage direction. However, the value of the gating charge was not affected by changes in pHi, suggesting that the effects of pHi on Po were not due to an alternation of the voltage sensitivity. At constant Vm, lowering pHi suppressed the [Ca2+]i-dependent channel activation and shifted the Po–[Ca2+]i relationship in the direction of higher [Ca2+]i with a reduction of maximal Po. Furthermore, both the mean open and mean closed times of the BK channels at pHi 6.3 in the presence of 10−4 M [Ca2+]i were shorter than those at pHi 7.3 in the presence of 10−5 M [Ca2+]i, even though these two different conditions gave a similar Po. The data indicate that cytoplasmic H+ suppresses Po of the BK channel in RPTECs, which involves the mechanism independent of Ca2+ activation. Our preliminary kinetic analysis also supported this notion.
  • Shih-Hurng Loh, Jong-Shiaw Jin, Chien-Sung Tsai, Chao-Ming Chao, Cheng ...
    2002 年 52 巻 3 号 p. 277-284
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    Intracellular pH (pHi) is a major homeostatic system within the cell. Changes in pHi exert great influence on cardiac contractility and rhythm. Both the housekeeping Na+–H+ exchanger (NHE) and the Na+–HCO3 symporter (NHS) have been confirmed as major transporters for the active acid extrusion mechanism in animal cardiomyocytes. However, whether the NHE and NHS functionally coexist in human ventricular cardiomyocytes remains unclear. We therefore examined the mechanism of pHi recovery following an NH4Cl-induced intracellular acidosis in the human ventricular myocardium. The pHi was monitored by microspectrofluorimetry by the use of intracellular 2',7'-bis(2-carboxyethyl)-5(6)-carboxy-fluorescein (BCECF)–fluorescence. HOE 694 (30 μM), a specific NHE inhibitor could block pHi recovery from induced intracellular acidosis completely in nominally HCO3-free HEPES Tyrode solution, but it only partially inhibited the pHi recovery in 5% CO2/HCO3 Tyrode solution. In 5% CO2/HCO3 Tyrode solution, the addition of HOE 694 together with DIDS (an NHS inhibitor) or the removal of [Na+]o could entirely inhibit the acid extrusion. We conclude for the first time that two different acid extruders, HCO3-independent and -dependent, were most likely the NHE and NHS, respectively, that functionally coexisted in the human ventricular cardiomyocytes.
  • Atsushi Kazama, Fumitaka Ikomi, Yasuaki Yashiro, Toshio Ohhashi
    2002 年 52 巻 3 号 p. 285-291
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    We examined the responses of pressurized bovine retinal functional arterioles (97–185 μm in diameter and ≈3 mm long) to vasoactive substances and the mode of action of acetylcholine (ACh) on the pressurized arterioles. The retinal arterioles were cannulated at both ends with glass micropipettes and perfused at a constant pressure of 60 mmHg. Vasoconstrictions of the retinal arterioles were induced by prostaglandin F (PG F), U46,619, noradrenaline (NA), and 5-hydroxytryptamine (5-HT) in a dose-dependent manner. The decreasing order of potency (pD2 value) in the constrictive responses was as follows: 5-HT = U46,619 > NA > PG F. On the other hand, sodium nitroprusside (SNP), isocarbacyclin (a stable prostaglandin I2 analog), ACh, and isoproterenol (ISP) caused dose-dependent vasodilatation in the pressurized retinal arterioles preconstricted with high-potassium solution (40 mM K+). The decreasing order of potency in the vasodilative responses was as follows: isocarbacyclin > SNP > ACh. The ACh-induced vasodilatation was suppressed significantly by pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME) (3 × 10−5 M). A treatment with L-arginine (10−3 M) in the presence of 3 × 10−5 M L-NAME reversed completely the L-NAME–induced reduction of the vasodilatation. These results suggest that ACh causes the production and release of endogenous nitric oxide or its related compounds, which results in vasodilatation of the pressurized bovine retinal functional arterioles.
  • Yoshiyuki Hirayama, Akinori Kuruma, Masayasu Hiraoka, Seiko Kawano
    2002 年 52 巻 3 号 p. 293-300
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    Ca2+-activated Cl current (ICl(Ca)) is activated by Ca2+ transient via Ca2+-induced Ca2+ release from sarcoplasmic reticulum in cardiac myocytes and is supposed to play an important role in the repolarization of action potential. It is not well understood, however, how ICl(Ca) is modulated to affect action potential in normal or pathological conditions. In this study we examined the effects of external acidosis on ICl(Ca) and action potential. A whole-cell patch clamp was performed to record action potential and ICl(Ca), using isolated rabbit ventricular myocytes. In the standard solution at pH 7.4, action potential duration (APD) was markedly prolonged by lowering the extracellular Cl concentration ([Cl]o) or by applying an anion channel blocker, 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS). In the low pH solution at 6.4, APD was markedly shortened and the amplitude of ICl(Ca) was increased at all membrane potentials. At pH 6.4, the apparent steady-state inactivation curves of ICl(Ca) were shifted to more positive potentials compared with those at pH 7.4, but no change in inactivation occurred at a holding potential of −60 mV. The apparent activation curves were not changed between the two sets of conditions. When ICl(Ca) was inhibited at low pH, early afterdepolarizations and triggered activities were induced. The amplitude of ICl(Ca) was suggested to be enhanced by the external acidosis, which may have prevented the induction of early afterdepolarization or triggered activity.
  • Chie Sato, Masahito Nemoto, Mamoru Tamura
    2002 年 52 巻 3 号 p. 301-312
    発行日: 2002年
    公開日: 2004/06/19
    ジャーナル フリー
    Incorporating the wavelength dependence of the scattering effect into a simple linear multicomponent analysis of intrinsic optical signals, we have reexamined the change in the hemoglobin (Hb) concentration and the origins of intrinsic signals in somatosensory cortex evoked with electrical stimulation of the hind limb (5 Hz, 2 s) of anesthetized rat. The concept of the analysis was to separate the effect of light scattering involved in the observed optical signals into two factors, light attenuation and modification of Hb absorption as a result of the wavelength dependence of the optical path length. This dependency was experimentally assessed with a tissue-simulating phantom whose absorption spectra were nearly identical to those of cerebral tissue through a thinned skull window in vivo. Using those phantom spectra, we carried out a curve fitting of the reflection spectra from the rat somatosensory cortex activated with an electrical stimulation of hind limb (5 Hz, 2 s). Oxygenated Hb slightly decreased at 0.5–1.5 s after an onset of the stimulus followed by an increase, which peaked at 4 s. Deoxygenated Hb increased at 1.0–1.5 s followed by a large late decrease. We again confirmed an early increase in the concentration of deoxygenated Hb in the rat somatosensory cortex after stimulation of the hind limb.
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