The Japanese Journal of Physiology
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Volume 53, Issue 6
Displaying 1-13 of 13 articles from this issue
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Regular Papers
  • Metabolic Modulation of Muscle Fiber Properties Unrelated to Mechanical Stimuli
    Yoshinobu Ohira, Fuminori Kawano, Roland R. Roy, V. Reggie Edgerton
    2003 Volume 53 Issue 6 Pages 389-400
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.389
    JOURNAL FREE ACCESS
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    The effects of chronically increasing (creatine-fed) or decreasing (β-guanidinopropionic acid [β-GPA]–fed) high-energy phosphates for up to 8 weeks on daily voluntary activity levels, swimming endurance capacity, electromyogram (EMG) activity, and the morphological and metabolic properties of single fibers in the soleus and extensor digitorum longus (EDL) muscles in young rats were determined. High-energy phosphate, voluntary activity, and soleus-integrated EMG levels were lower in β-GPA–fed rats than in control rats. Endurance capacity was higher at a relatively low intensity of swimming and lower at a relatively high intensity in β-GPA–fed rats than in control rats. Muscle mass and fiber size were smaller, and the percentage of slow fibers was higher in the soleus and EDL of β-GPA–fed rats than in control rats. Succinate dehydrogenase activity was higher in both the fast and slow fibers of the EDL of β-GPA–fed rats than in control rats. Thus, a reduction in high-energy phosphates transformed some fast fibers toward a slow phenotype. Creatine supplementation had minimal effects: The only significant change was an increase in α-glycerophosphate dehydrogenase activity in the fast fibers of the EDL. These results indicate that the metabolic environment of a muscle fiber can influence the prominence of a given muscle fiber independent of the activity level of muscle.
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  • The Influences of L(+)-Lactate and pH on Contractile Performance in Rabbit Glycerinated Skeletal Muscle
    Shin-ichi Miyake, Yoshiki Ishii, Takashi Watari, Zhenli Huang, Teizo T ...
    2003 Volume 53 Issue 6 Pages 401-409
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.401
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    To know whether L(+)-lactate directly induces the decrease in muscle contractile performance, several parameters of cross-bridge function were measured at various concentrations of lactate and pH in glycerinated rabbit psoas and soleus muscles at three different temperatures (5, 20, 28°C). At all pHs studied (pH 7.0, 6.5, 6.0, and 5.5), isometric tension, unloaded velocity of shortening, and stiffness of a fiber during active and resting state in the presence of 50 mM lactate were not virtually different from those in the absence of lactate, but pH had remarkable effects on these parameters. The active stiffness decreased only slightly, and the small resting stiffness appeared at low pH; they were not affected by the presence of lactate. The present results indicate that the lactate anions may not have marked influence on the interaction between actin and myosin, and the concomitant change in pH with the production of lactate may remarkably affect it, as far as they were examined under the existing conditions of the experimental solutions.
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  • Hyperthyroidism Causes Mechanical Insufficiency of Myocardium with Possibly Increased SR Ca2+-ATPase Activity
    Koh Takeuchi, M. Minakawa, M. Otaki, S. Odagiri, K. Itoh, A. Murakami, ...
    2003 Volume 53 Issue 6 Pages 411-416
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.411
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    Hyperthyroidism is known to affect multiple organ functions, and thyroid hormone has been known to improve myocardial function in a failing heart. The purpose of this study is to elucidate the functional and metabolic effects of thyroid hormone on myocardium in a rat model exposed to long-term excess thyroid hormone, particularly focusing on the SR Ca2+-ATPase (SERCA2) function. 3,5,3'-Triiodo-L-thyronine (T3), or the vehicle, was subcutaneously given for 4 weeks (T3 and control [C] group). Bolus I.V. Thapsigargin (TG) was used to test the SERCA2 function (C-TG and T3-TG) in Langendorff perfused heart. Myocardial functions such as LV-developed pressure (LVDP; mmHg), ± dP/dt (mmHg/s), τ (ms), and oxygen consumption (MVO2; ml/min/g wt) were measured. SERCA2 and GLUT4 protein level were also evaluated by Western immunoblotting. Left ventricle to body weight (LV/BW) ratio was significantly higher in the T3 group. Both negative dP/dt and τ were significantly decreased by TG. It is interesting that the decrement of negative dP/dt and τ attained by TG was significantly larger in the hyperthyroid group (T3-TG) than in a normal heart (C-TG). SERCA2 and GLUT4 protein levels were not significantly different between control and the T3 group. We conclude that prolonged exposure to thyroid hormone causes hypertrophy of the myocardium and an augmentation of the SR Ca2+ ATPase activity. Care must be taken in hyperthyroid heart during the ischemia-reperfusion process where the SRECA2 function is inhibited.
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  • Block of Recombinant KCNQ1/KCNE1 K+ Channels (IKs) by Intracellular Na+ and Its Implications on Action Potential Repolarization
    Minako Orikabe, Yuji Hirano, Mitsuaki Isobe, Masayasu Hiraoka
    2003 Volume 53 Issue 6 Pages 417-425
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.417
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    IKs, the slow component of delayed rectifier K+ current, plays an important role for the repolarization of ventricular action potential. We investigated the block of IKs by intracellular Na+ ([Na+]i), using a heterologous expression system (KCNQ1/KCNE1 expressed in COS7 cells), since this well-known blocking action on various K+ channels has not been fully or quantitatively characterized in IKs current. The Na+ block of IKs was concentration- and voltage-dependent and was described by a conventional binding-site model (Woodhull AM: J Gen Physiol 61: 687–708, 1973). In physiological ionic conditions, the blocking action was operating noticeably with Δ ("electrical" distance of the block site) ∼0.6 and Kd(0) (apparent dissociation constant at 0 mV) ∼300 mM. Because Kd(0) was a function of intra- and extracellular K+ concentrations, changes in ionic environments not only of [Na+]i, but also of [K+]o, affected the amplitude of IKs through the modulation of the Na+ block. Based on these experimental data, we analyzed the effects of Na+ block on action potentials by a computer simulation study, using the Luo-Rudy model. In a physiological ionic environment, the Na+ block of IKs contributed little to modifying action potentials. However, when action potential duration (APD) was marginally prolonged because of decreased IKs, as observed in M cells under the conditions of bradycardia and low [K+]o, the Na+ block of IKs may contribute to arrhythmogenesis through the facilitation of early afterdepolarizations (EADs).
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  • Effect of Skin Temperature on the Cholinergic Sensitivity of the Human Eccrine Sweat Gland
    Dana M. DiPasquale, Michael J. Buono, Fred W. Kolkhorst
    2003 Volume 53 Issue 6 Pages 427-430
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.427
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    Although sweat gland activity is directly controlled by the central nervous system, which detects changes in core body temperature, sweat glands can also be influenced by local cutaneous thermal conditions. Objective: The present study sought to determine the effect of local skin temperature on pilocarpine-induced sweating within a range of typical skin temperatures. Methods: Thirteen subjects (30 ± 6 years; 172 ± 11 cm; 72.8 ± 11.0 kg) had forearm sweat rates measured at rest following pilocarpine iontophoresis at each of three skin temperatures in randomized order: warm (Twarm = 37.1 ± 0.9°C), control (Tcon = 32.3 ± 1.4°C), and cool (Tcool = 26.6 ± 1.3°C). Tskin was raised and lowered with an electric heating pad and gel ice pack, respectively. Forearm Tskin was measured with a skin temperature probe. Pilocarpine iontophoresis was used on an approximately 7 cm2 area of the anterior forearm to stimulate localized sweating. Following stimulation, sweat was collected from the area for 15 min with a Macroduct Sweat Collection System. Results: There was a higher sweat rate at Twarm (p = 0.001) and Tcon (p = 0.006) compared to that at Tcool. However, there was no difference between the sweat rate at Twarm and that at Tcon (p = 0.127). Conclusion: These results indicated that skin temperatures below approximately 32°C affect local sweat production primarily by altering glandular sensitivity to the neurotransmitter, whereas skin temperatures above approximately 32°C predominantly affect neurotransmitter release. Furthermore, sweat glands display maximal or near maximal cholinergic sensitivity at resting skin temperature in a thermoneutral environment.
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  • Modulation of Intracellular Na+ and Ca2+ Induced by the Cardiac Na+-Ca2+ Exchanger in Guinea Pig Ventricular Myocytes
    A. Yoshida, A. Noma, T. Powell
    2003 Volume 53 Issue 6 Pages 431-442
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.431
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    The Na+-Ca2+ exchanger current was measured in single guinea pig ventricular myocytes, using the whole-cell voltage-clamp technique, and intracellular free calcium concentration ([Ca2+]i) was monitored simultaneously with the fluorescent probe Indo-1 applied intracellularly through a perfused patch pipette. In external solutions, which have levels of Ca2+ (∼66 μM Ca2+) thought low enough to inhibit exchanger turnover, the removal of external Na+ (by replacement with Li+) induced both an outward shift of the holding current and an increase in [Ca2+]i, even though the recording pipette contained 30 mM bis(O-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA), sufficient to completely block phasic contractions. The effects of Na+ removal were blocked either by the extracellular application of 2 mM Ni2+ or by chelating extracellular Ca2+ with 1 mM EGTA. In the presence of 10 μM Ryanodine, the effects of external Na+ substitution with Li+ on both membrane current and [Ca2+]i were attenuated markedly in amplitude and at a much slower time course. Reversal potentials were estimated by using ramp pulses and by defining exchange currents as the Ni2+-sensitive components. The experimental values of the reversal potential and [Ca2+]i were used to calculate cytosolic Na+ ([Na+]i) by assuming an exchanger stoichiometry of 3Na+ : 1Ca2+. These calculations suggested that in the nominal absence of external Ca2+ (∼66 μM under our experimental conditions), the exchanger operates at −40 mV as though ∼40 mM Na+ had accumulated in the vicinity of the intracellular binding sites. We conclude that under the conditions of low extracellular Ca2+ and high intracellular Ca2+ buffering, the Na+-Ca2+ exchanger can still generate sufficient Ca2+ influx on the removal of external Na+ to markedly increase cytosolic free Ca2+.
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  • Central Administration of Ghrelin Stimulates Pancreatic Exocrine Secretion via the Vagus in Conscious Rats
    Norikazu Sato, Setsuko Kanai, Saeko Takano, Mieko Kurosawa, Akihiro Fu ...
    2003 Volume 53 Issue 6 Pages 443-449
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.443
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    Ghrelin, a novel growth-hormone releasing peptide, was originally isolated from rat and human stomach. Immunohistochemical analyses revealed that ghrelin-immunoreactive neurons were localized in the hypothalamic arcuate nucleus. The function of the digestive organs is controlled from the central nervous system, and the vagus nerve plays an important role. Intracerebroventricular and intravenous administration of ghrelin significantly increased gastric acid secretion, and its effect was abolished by vagotomy. In the present study, the effect of centrally injected ghrelin on pancreatic exocrine secretion was examined in conscious rats. Moreover, an electrophysiologic study was conducted in anesthetized rats to examine whether the excitation of vagal efferent nerve could be induced by ghrelin. To determine the pancreatic exocrine secretion, rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted in conscious rats on day 4 or 5 after the operation. To exclude the involvement of gastric acid, a proton pump inhibitor omeprazole (5 μmol/kg) was administered into the duodenum 1 h before ghrelin injection. An intracerebroventricular administration of ghrelin (12, 60, and 300 pmol/10 μl) significantly increased pancreatic fluid and protein output in a dose-dependent manner. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central ghrelin. In contrast, an intravenous injection of ghrelin (300 pmol/10 μl) had no effect. Centrally administered ghrelin stimulated the vagal efferent nerve in anesthetized rats. In conclusion, centrally administered ghrelin stimulates pancreatic exocrine secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid secretion.
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  • High-Glucose Induced Protective Effect against Hypoxic Injury Is Associated with Maintenance of Mitochondrial Membrane Potential
    Min Hwa Kim, Yi-Sook Jung, Chang-Hyun Moon, Soo Hwan Lee, Eun Joo Baik ...
    2003 Volume 53 Issue 6 Pages 451-459
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.451
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    Our previous report has showed that the treatment of 48 h with 22 mM glucose prevents hypoxia-induced cardiac cell death. In the present study, we investigated whether high glucose affects the mitochondrial death pathway during hypoxia, and if it does, what relates to the high glucose induced cardioprotection. Heart-derived H9c2 cells were incubated in low (5.5 mM) or high (22 mM) glucose medium for 48 h, then transferred to a normoxic or hypoxic condition. The hypoxia-induced reduction of mitochondrial redox potential, assessed by MTT assay, was inhibited in high glucose treated cells. The mitochondrial membrane potential was significantly decreased by hypoxia in low glucose treated cells, but not in high glucose treated cells. The hypoxia-induced cytoplasmic accumulation of cytochrome c, released from the mitochondria, was blocked by a treatment of high glucose. High glucose did not induce the expression of an antiapoptotic protein Bcl-2, nor did it reduce a proapoptotic protein Bax, but it did inhibit a hypoxia-induced downregulation of Bcl-2. The cellular ATP contents were not changed by the treatment of high glucose for 48 h, and the hypoxia-induced decline of intracellular ATP level was observed in high glucose treated cells and in low glucose. A glycolytic inhibitor, 2-deoxyglucose, did not reverse the high glucose induced reduction of LDH release. The elevation of [ROS]i induced by hypoxia was inhibited in high glucose treated cells. These results suggest that high glucose induced cardioprotection may be accounted for in part by the preservation of MMP and the maintenance of a basal level of [ROS]i during hypoxia.
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  • Carotid-Sinus Baroreflex Modulation of Core and Skin Temperatures in Rats: An Open-Loop Approach
    Dongmei Zhang, Motonori Ando, Fumiyasu Yamasaki, Takayuki Sato
    2003 Volume 53 Issue 6 Pages 461-466
    Published: 2003
    Released on J-STAGE: June 01, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.53.461
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    The neural mechanisms of the thermoregulatory control of core and skin temperatures in response to heat and cold stresses have been well clarified. However, it has been unclear whether baroreceptor reflexes are involved in the control of core and skin temperatures. To investigate how the arterial baroreceptor reflex modulates the body temperatures, we examined the effect of pressure changes of carotid sinus baroreceptors on core and skin temperatures in halothane-anesthetized rats. To open the baroreflex loop and control arterial baroreceptor pressure (BRP), we cut vagal and aortic depressor nerves and isolated carotid sinuses. We sequentially altered BRP in 20-mmHg increments from 60 to 180 mmHg and then in 20-mmHg decrements from 180 to 60 mmHg while measuring systemic arterial pressure (SAP), heart rate (HR), and core blood temperature (Tcore) at the aortic arch and skin temperature (Tskin) at the tail. In response to the incremental change in BRP by 120 mmHg, SAP, HR, and Tcore fell by 90.3 ± 5.1 mmHg, 60.3 ± 10.5 beats min−1, and 0.18 ± 0.01°C, respectively. Tskin rose by 0.84 ± 0.10°C. The maximum rate of change per unit BRP change was −2.1 ± 0.2 for SAP, −1.5 ± 0.4 beats min−1 mmHg−1 for HR, −0.003 ± 0.001°C mmHg−1 for Tcore, and 0.011 ± 0.002°C mmHg−1 for Tskin. After the administration of hexamethonium or bretylium, these baroreflexogenic responses were completely abolished. We concluded that Tcore and Tskin are modulated by the arterial baroreceptor reflex.
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