The Japanese Journal of Physiology
Print ISSN : 0021-521X
Volume 54, Issue 4
Displaying 1-13 of 13 articles from this issue
Review
  • K. Harada, S. Morimoto
    2004 Volume 54 Issue 4 Pages 307-318
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Troponin, one of the sarcomeric proteins, plays a central role in the Ca2+ regulation of contraction in vertebrate skeletal and cardiac muscles. It consists of three subunits with distinct structure and function, troponin T, troponin I, and troponin C, and their accurate and complex intermolecular interaction in response to the rapid rise and fall of Ca2+ in cardiomyocytes plays a key role in maintaining the normal cardiac pump function. More than 200 mutations in the cardiac sarcomeric proteins, including myosin heavy and light chains, actin, troponin, tropomyosin, myosin-binding protein-C, and titin/connectin, have been found to cause various types of cardiomyopathy in human since 1990, and more than 60 mutations in human cardiac troponin subunits have been identified in dilated, hypertrophic, and restrictive forms of cardiomyopathy. In this review, we have focused on the mutations in the genes for human cardiac troponin subunits and discussed their functional consequences that might be involved in the primary mechanisms for the pathogenesis of these different types of cardiomyopathy.
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Regular Papers
  • J. Mizuno, S. Mohri, J. Shimizu, S. Suzuki, T. Mikane, J. Araki, T. Ni ...
    2004 Volume 54 Issue 4 Pages 319-329
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Intramyocardial Ca2+ recirculation fraction (RF) critically determines the economy of excitation-contraction coupling. RF is obtainable from the exponential decay of the postextrasystolic potentiation of left ventricular (LV) contractility. We have shown that RF remains unchanged despite increasing LV volume (LVV) at normothermia, but decreases with increasing temperature at a constant LVV. However, it remains unknown whether the temperature-dependent RF was not due to the simultaneously changed peak LV pressure (LVP) at a constant LVV. We hypothesized that this temperature-dependent RF would be independent of the simultaneous change in LVP. We used nine excised, cross-circulated canine hearts and allowed their LVs to contract isovolumically. During stable regular beats at 500 msec intervals, we inserted an extrasystolic beat at 360 msec interval followed by the postextrasystolic beats (PESs) at 500 msec intervals. We equalized the temperature-dependent peak LVPs of the regular beats at 36°C and 38°C to the peak LVP level of the stable regular beat at 33°C by adjusting LVV. We fitted the same equation: nEmax = a exp[−(i − 1)/τe] + b exp[−(i − 1)/τs]cos[π(i − 1)] + 1, used before to the normalized Emax (maximum elastance) values of PESi (i = 1–6) relative to the regular beat Emax. RF given by exp(−1/τe) decreased by 19% to 38°C from 33°C. The temperature coefficient (Q10) of 1/RF was significantly greater than 1.3. The present results indicated a similar temperature dependence of RF and its Q10 to those we observed previously without equalizing peak LVP. Thus, the temperature-dependent RF is independent of ventricular loading conditions.
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  • J.H. Lee, E.Y. Han, M.S. Kang, F. Kawano, H.J. Kim, Y. Ohira, C.K. Kim
    2004 Volume 54 Issue 4 Pages 331-337
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    The effects of 20 weeks of intermittent cold-water-immersion on myosin heavy chain (MHC) expression,cross-sectional area (CSA), myonuclear number, andmyonuclear domain size in isolated single fiber of soleusand extensor digitorum longus (EDL) muscles were studied inmale Wistar rats. Cold exposure was accomplished bysubmerging the rats in shoulder-deep water, maintained at∼18°C, for 1 hour/day, 5 days/week and for 20 weeks.Cold exposure resulted in a significant inhibition of bodyand soleus muscle weight gain. The percent type IIa MHCfibers of EDL muscle was increased, whereas that of type IIa+ b MHC fibers was less in cold-exposed group than controls(p < 0.05). The mean CSA and myonuclear number intype I MHC fibers of soleus muscle in cold-exposed groupwere significantly less than controls. Myonuclear domain intype IIa fibers of EDL in the cold-exposed group was greaterthan controls (p < 0.05). It is suggested thatprolonged cold exposure causes the fiber-type-specificadaptation in rat hindlimb muscles. It is further indicatedthat cold-exposure-related modulation of myonuclear numberwas closely related to reduction of fiber CSA, not the shiftof fiber phenotype.
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  • Y. Takemoto
    2004 Volume 54 Issue 4 Pages 339-345
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    The neurotransmitter candidate L-proline elicits changes in the cardiovascular system via actions in the brainstem. However, its action have not yet been determined in the ventrolateral medulla (VLM), a brain region critical in mediating vasomotor sympathetic nervous system responses. Microinjections of L-glutamate produce depressor responses in the caudal (C) VLM, but pressor responses in the rostral (R) VLM and the caudal pressor area (CPA) in the far caudal CVLM. The present study tested whether microinjections of l-proline in the VLM produce a pattern of hemodynamic responses distinct from that of l- glutamate. Urethane-anesthetized rats received arterial catheters and were implanted with flow probes around the abdominal aorta (supplies hindquarters). The surface of each rat's VLM was then exposed. L-Proline induced dose- dependent depressor responses in the CVLM (0.003–1.0 M, 34 nl), but did not induce hemodynamic responses in sites of the RVLM (0.01–1.0 M, 34 nl) that responded to L-glutamate (0.01 M, 34 nl). L-Proline injections (0.1 M, 34 nl) induced rapid and consistent depressor responses correlated with coincident decreases in hindquarter resistance (arterial blood pressure/flow) in the CVLM and CPA, but only inconsistent responses in a few sites in the RVLM. In summary, L-proline induced a distinct pattern of depressor responses preferentially in caudal regions of the VLM, and these depressor effects were associated with decreases in hindquarter resistance. These findings indicate that l-proline may have unique roles including cardiovascular regulation independently from L-glutamate, especially in caudal region of the VLM, via a mechanism that involves altering hindquarter resistance.
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  • Stefan F.J. Langer
    2004 Volume 54 Issue 4 Pages 347-356
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    The decelerative part of the left ventricular isovolumic pressure decay is an important phase to make the heart ready for diastolic refill (lusitropy). Its widely used characterization by an exponential regression with zero pressure asymptote or coestimated asymptote provides empirically biased time constant estimates because of significant deviations of the pressure decay from exponentiality. We systematically analyzed the regression residua of these pressure decays in isolated ejecting rat, guinea pig, and ferret hearts. A four-parametric logistic (tangens hyperbolicus) function, together with a superimposed acustomechanic oscillation, yields normally distributed residua with standard regression error typically less than one per cent of the initial pressure; this is the first model with proved unbiased and statistically complete regressive extraction of the information provided by the time course of pressure decay. Equal values of the lusitropic parameters (logistic time constant and pressure asymptote) were estimated even after the oscillatory component was removed from the regression model. Reliable estimates of the frequency, but not of the amplitude, can be obtained by fitting the oscillation model to the residua provided by the logistic; this two-step method is statistically weaker than the full one-step model, but it reduces computational effort. In conclusion, the four-parametric logistic, but not a three-parametric exponential or logistic model, suffices to obtain unbiased lusitropic parameters characterizing the left ventricular isovolumic pressure decay of small animal hearts.
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  • Shih-Wei Chou, Li-Ling Chiu, Yu-Min Cho, Hsin-Yi Ho, John L. Ivy, Chun ...
    2004 Volume 54 Issue 4 Pages 357-363
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Altitude training is a common method used to enhance endurance performance in athletes. We have examined the interactive effect of exercise training and chronic hypoxic on glycogen storage and GLUT4 protein expression in cardiac muscles. Thirty-two male Sprague- Dawley rats were weight balanced and assigned to one of the following four groups: control, exercise, hypoxia, and hypoxia-exercise. Rats with hypoxic treatment (breathing 14% O2 for 12 hr/d) were exposed under normobaric conditions. The training protocol consisted of swimming for two 3-hr periods per day for 4 weeks. Glycogen content, GLUT4 protein, and mRNA of all rats were determined 16 hr after treatments. Four-week exercise training without hypoxia significantly elevated myocardial glycogen level by 45%. The chronic hypoxic-exercise training elevated the myocardial glycogen level by 67% above control level, significantly greater than the exercise group. Chronic hypoxia, exercise training, and hypoxia-exercise training significantly elevated GLUT4 protein by 40–70% in cardiac muscles. Chronic hypoxia significantly elevates the GLUT1 protein level independent of exercise training. The new finding in this study was that GLUT4 gene expression in cardiac muscle can be stimulated by exercise training with hypoxia treatments. This molecular adaptation appears to be associated with the observed increase in glycogen storage of the muscle.
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  • H. Itohara, S. Sasaki, T. Fu, I. Nakagaki, S. Hori, H. Tateishi, S. Ma ...
    2004 Volume 54 Issue 4 Pages 365-371
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    We performed peripheral nerve allografting in rats with spinal cord injury, and measured motor function and axonal membrane potential as well as Ca2+ concentration of the nerve grafting spinal cord area by using a behavior observation system and a confocal laser-scanning microscope, respectively. In our experiments, we produced a model of peripheral nerve grafting after spinal cord injury by peripheral nerve allografting (sciatic nerve) in rats with spinal cord injury (thoracic cord hemisection). The group with spinal cord injury that underwent peripheral nerve grafting showed improvement in motor function, a significant increase in the axonal action potential, and a slight increase in the Ca2+ concentration compared with the group that did not undergo nerve grafting.
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  • G. Iribe, J. Shimizu, S. Mohri, Yi Syuu, T. Imaoka, T. Kiyooka, J. Ara ...
    2004 Volume 54 Issue 4 Pages 373-383
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    We have previously found that the postextrasystolic (PES) potentiation (PESP) of the left ventricular (LV) contractility (Emax) decays typically in transient alternans even in the normally ejecting canine heart. This contradicted the general expectation that arterial pressure (AP) and LV pressure (LVP) usually decay exponentially during PESP. We hypothesized this contradiction to be due to the different cardiodynamic behaviors of AP and LVP from LV Emax during PESP. We tested this hypothesis by measuring AP, LVP, LV volume, Emax, effective arterial elastance (Ea) as an index of afterload, and pulse pressure (PP) during PESP in eight anesthetized open-chest dogs by using the conductance catheter system. We changed Ea by changing the total peripheral resistance (TPR) with methoxamine hydrochloride (iv) and repeated the measurements. Although the Emax alternans patterns during PESP were comparable between the normal and high afterloads, LVP and PP were slightly potentiated and alternated under the normal afterload, whereas LVP and PP were obviously potentiated and alternated under the high afterload. We also simulated the effects of Ea/Emax on the transient alternans of AP and LVP on a computer. Despite the same alternans pattern of Emax, a higher Ea/Emax, which is typical in heart failure, caused a larger PP alternans, whereas a lower Ea/Emax, which is typical in normal hearts, almost eliminated it. These results suggest that a transient alternans of LV contractility during PESP could be overlooked when AP and LVP are monitored in in situ normal hearts.
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  • S. Miyazaki, S. Iwase, T. Mano, H. Fukuda, J. Mochida
    2004 Volume 54 Issue 4 Pages 385-393
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Investigations of the Ia afferent discharge in clarifying problems in disused and malused skeletal muscles have been carried out mainly in muscles of the upper extremities. However, such problems actually occur more frequently in the antigravity muscles of the lower extremities, such as the triceps surae muscle. An analysis of microneurographically recorded Ia discharges from the tibial nerve innervating the triceps surae muscle during dynamic movement of the ankle joint indicated that they mainly transmitted information on the angular velocity of the joint. However, the information on the position sense of the joint was not as well transmitted through Ia discharges. There was no correlation between the joint angle and the static response. However, the dynamic response of a Ia afferent was well correlated to the angular velocity. It is concluded that the human proprioception of the triceps surae muscle was not dependent on the position of the ankle joint, but largely on its movement by the stretching of the muscle.
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  • K. Kashihara, T. Kawada, Meihua Li, M. Sugimachi, K. Sunagawa
    2004 Volume 54 Issue 4 Pages 395-404
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Although the Bezold-Jarisch (BJ) reflex is potentially evoked during acute myocardial ischemia or infarction, its effects on the static characteristics of the arterial baroreflex remain to be analyzed in terms of an equilibrium diagram between the neural and peripheral arcs. The neural arc represents the static input-output relationship between baroreceptor pressure input and efferent sympathetic nerve activity (SNA), whereas the peripheral arc represents that between SNA and arterial pressure (AP). In 8 anesthetized rabbits, we increased carotid sinus pressure stepwise from 40 to 160 mmHg in increments of 20 mmHg at one-minute intervals while measuring renal SNA and AP under control conditions and during the activation of the BJ reflex by intravenous administration of phenylbiguanide (PBG, 100 μg kg−1 min−1). The neural arc approximated a sigmoid curve whereas the peripheral arc approximated a straight line. PBG decreased AP at the operating point from 91.3 ± 2.4 to 71.7 ± 3.1 mmHg (P < 0.01), and attenuated the total loop gain at the operating point from −1.31 ± 0.44 to −0.51 ± 0.14 (P < 0.05). The equilibrium diagram indicated that PBG caused a parallel shift of the neural arc toward lower SNA such that the maximum SNA was reduced to approximately 60% of control. PBG decreased neural and peripheral arc gains at the operating point to approximately 43% and 77%, respectively. In conclusion, the BJ reflex blunts arterial baroreflex via the shift of the neural arc toward lower SNA.
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  • Mi Jeong Kim, Chang-Hyun Moon, Mi-Young Kim, Min Hwa Kim, Soo Hwan Lee ...
    2004 Volume 54 Issue 4 Pages 405-414
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    In the present study, we investigated the role of protein kinase C (PKC) isoforms during hypoxia in heart-derived H9c2 cells. Hypoxia caused a rapid translocation of PKC-δ from soluble to particulate fraction and a downregulation of PKC-ε and PKC-ζ, whereas PKC-α and PKC-βI remained unaltered. When H9c2 cells were pretreated with PKC-δ inhibitor rottlerin (3 μM), hypoxia-induced apoptotic and necrotic cell death were significantly increased. Hypoxic insult also caused an activation of extracellular signal-regulated protein kinase (ERK) and p38 MAPK with no change in c-Jun NH2-terminal protein kinase (JNK) phosphorylation. Hypoxia-induced cell death was increased by treatment with ERK1/2 inhibitor U0126 (10 μM), but attenuated by p38 MAPK inhibitor SB202190 (10 μM). Treatment with rottlerin completely blocked the hypoxia-induced ERK phosphorylation, whereas it significantly increased p38 MAPK phosphorylation. The hypoxia-induced translocation of PKC-δ was not altered by U0126 and/or SB202190. From these results, it is suggested that hypoxia causes a rapid translocation of PKC-δ and subsequently ERK activation and p38 inactivation, rendering H9c2 cells resistant to hypoxia-induced cell death.
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Short Communication
  • A. Ikari, K. Nakajima, Y. Suketa, H. Harada, K. Takagi
    2004 Volume 54 Issue 4 Pages 415-419
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Renal epithelial cells may have Mg2+ transport pathways that regulate intracellular free Mg2+ concentration ([Mg2+]i) and reabsorption into the body. In mag-fura 2 fluorescent measurement, extracellular Mg2+ removal induced a Na+-independent [Mg2+]i decrease. The [Mg2+]i decrease was suppressed by methyl arachidonyl fluorophosphonate, a cytosolic and Ca2+-independent phospholipase A2 (iPLA2) inhibitor, and bromoenol lactone, an iPLA2 inhibitor, but it was not suppressed by a secretory phospholipase A2 inhibitor. On the contrary, the [Mg2+]i decrease was enhanced by the addition of exogenous arachidonic acid (AA). Next, we examined the effect of AA metabolite inhibitors on the [Mg2+]i decrease. 17-octadecynoic acid inhibited the [Mg2+]i decrease, but indomethacin and nordihydroguaiaretic acid did not. In the 17-octadecynoic acid-treated cells, 20-hydroxy-(5Z,8Z,11Z,14Z)-eicosatetraenoic acid (20-HETE) recovered the [Mg2+]i decrease. Nicardipine inhibited both the basal and the 20-HETE-enhanced [Mg2+]i decrease. These results suggest that 20-HETE is a key mediator in the activation of Na+-independent Mg2+ efflux.
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Technical Note
  • D.G. Le Couteur, Z.L. Yin, A.J. McLean, L.P. Rivory
    2004 Volume 54 Issue 4 Pages 421-429
    Published: 2004
    Released on J-STAGE: January 06, 2005
    JOURNAL FREE ACCESS
    Wash-in experiments, which may be useful for the study of the disposition of substrates in the liver, have not been well described. To investigate physiological models for wash-in curves, we performed experiments on the perfused livers of male Wistar rats anesthetized with pentobarbital. Test perfusate contained 14C-sucrose as the extracellular marker and 3H-glucose. Liver perfusions were performed with background glucose concentrations of 5.7, 10.7, 51.2, or 108.5 mM. Outflow time-activity curves were analyzed with the use of four models. The Vmax and Km for the influx of glucose were 1.1 ± 0.03 μmol/s/g and 41 ± 3 mM with the Crone- Renkin early extraction model; 1.4 ± 0.04 μmol/s/g and 36 ± 3 mM with dispersion model analysis; 1.8 ± 0.1 μmol/s/g and 25 ± 4 mM with the Goresky distributed model to fit differentiated wash-in curves; and 2.7 ± 0.6 μmol/s/g and 28 ± 21 mM with compartmental analysis. There was reasonable agreement between the four models, and they yielded results similar to those reported for glucose uptake in other preparations.
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