The Journal of Physiological Sciences
Online ISSN : 1880-6562
Print ISSN : 1880-6546
ISSN-L : 1880-6546
Volume 57, Issue 3
Displaying 1-8 of 8 articles from this issue
Regular Papers
  • Ryoichi Yoshimura, Shingo Somekawa, Hiroshi Omori, Yasuhisa Endo
    2007 Volume 57 Issue 3 Pages 139-145
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: April 20, 2007
    JOURNAL FREE ACCESS
    Vagal hyperactivity correlates with enhanced DNA synthesis and cell proliferation in the peripheral tissues of ventromedial hypothalamic (VMH)–lesioned rats. The infusion of an ACh receptor agonist, carbachol (Cch), induces rat duodenal and pancreatic cell proliferation to a degree comparable to the VMH lesions. Whereas the VMH lesions also induce the proliferation of hepatic cells, it is unclear whether Cch can also do this. Here we attempted to clarify the mechanism of hepatic cell proliferation induction by cholinergic stimulation. First, hepatic cell proliferation was examined in rats previously vagotomized and intraperitoneally administered with Cch via an osmotic minipump. Second, the sera from the Cch-infused rats were examined for a proliferative effect on isolated hepatic cells. And last, the effect of the presence of hepatic nonparenchymal cells (NPCs) on the proliferation of the cultured hepatocytes treated with Cch was investigated. Immunohistochemistry for proliferating cell nuclear antigen (PCNA) showed that the 3-day Cch infusion significantly increased the number of PCNA-immunoreactive cells in the liver. Moreover, the sera from the Cch-infused rats increased the number of PCNA-immunoreactive hepatocytes in culture. However, Cch alone did not induce proliferation in monocultured hepatocytes. When compared with the monoculture of hepatocytes, the coculture of those with hepatic NPCs resulted in enhanced PCNA immunoreactivity after a 4-day treatment with 3 mM Cch. These findings suggest that ACh induces hepatocyte proliferation, which is mediated by unidentified humoral factor(s) possibly secreted from hepatic NPCs, and that it also participates in liver hypertrophy in the VMH-lesioned animals.
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  • Yoshiakira Wakita
    2007 Volume 57 Issue 3 Pages 147-157
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: May 03, 2007
    JOURNAL FREE ACCESS
    Some improvements of Kodama's method for perfusing the isolated rabbit heart in its working mode were made. Increases in the right and left atrium pressure, together with an increase in the pulmonary artery pressure, were observed to occur immediately after the start of venous return, and then all of the increased pressures were found to remain at each constant level. In these stable states, the administration of dopamine (DA) into the perfusate was found to produce dose-related increases in contractile activities. In the preparations denervated with reserpine or 6-hydroxydopamine, in which tyramine (Ty) produced no response, the inotropic effectiveness of DA did not differ from that in the normal ones. On the other hand, responses to noradrenaline (NA) were found to increase significantly after the denervation. DA produced a dose-related increase in heart rates in the normal preparation, and this effect was greatly suppressed in the denervated preparations, suggesting that the primary chronotropic effect of DA is an indirect one via the release of NA from the sympathetic nerve terminals. Arrhythmogenic effects of NA, Ty or DA were also observed in these preparations. At all the doses tested, the incidence rates by NA were as high as 50% or more, the type of arrhythmia being recognized as atrial or ventricular extrasystole from the ECG analysis. On the other hand, the rates by DA were relatively low, less than 34%. From a comparison of the incidence rates between the normal and denervated preparations, this effect of DA was considered to be primarily an indirect one.
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  • Yong-Woon Kim, Keon-Ho Kim, Dong-Kuk Ahn, Hee-Sun Kim, Jong-Yeon Kim, ...
    2007 Volume 57 Issue 3 Pages 159-165
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: May 08, 2007
    JOURNAL FREE ACCESS
    We assessed the time course effects of lipopolysaccaride (LPS) on food intake, cytokines, and hormones in rats and evaluated the relation between LPS-induced anorexia and its possible causative factors. Food intake was reduced 2 h after LPS injection (500 μg/kg, intraperitoneally) and remained decreased for 24 h. Plasma TNF-α and IL-6 levels increased by LPS administration at 0.5 and 2 h, and at 2 and 4 h, respectively. Plasma leptin and glucose levels were elevated at 8 and 16 h, and insulin levels were elevated at 2, 4, 8, and 16 h in the LPS-injected group, as compared to the counterpart controls. IL-6 levels in the CSF were elevated at 2 and 4 h. Hypothalamic cytokines tended to increase as early as 0.5 h after LPS injection and remained increased until 16 h. LPS-induced anorexia was attenuated in insulin-deficient STZ rats and was abolished by insulin treatment. The hypothalamic expression of NPY, a target of insulin's anorexic effect, was decreased 2 h after LPS administration, and central NPY injection (3 nM) prevented LPS-induced anorexia. In conclusion, cytokines, insulin, and leptin levels evidence different time courses by LPS administration. In LPS-induced anorexia, insulin may constitute a newly found causative factor, whereas leptin appears to be uninvolved in an early period in rats.
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  • Hong-Guang Nie, Li-Ying Hao, Jian-Jun Xu, Etsuko Minobe, Asako Kameyam ...
    2007 Volume 57 Issue 3 Pages 167-173
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: May 22, 2007
    JOURNAL FREE ACCESS
    L-type Ca2+ channels have two opposing forms of autoregulatory feedback, Ca2+-dependent facilitation (CDF) and Ca2+-dependent inactivation (CDI), in response to increases in intracellular Ca2+ concentration. Calmodulin (CaM) has been reported to mediate the two feedbacks. Although both the direct binding of CaM and the phosphorylation mediated by Ca2+/CaM-dependent protein kinase II (CaMKII) have been suggested as underlying mechanisms, the detailed features remain to be clarified. In this study, we investigated the effects of CaM and CaMKII inhibitors on CDF and CDI with patch clamp cell-attached recordings in guinea-pig ventricular myocytes. We confirmed that a high-K+ and high-Ca2+ could induce an increase of the intracellular Ca2+ concentration and subsequent CDF and CDI. We then found that CDF and CDI were both depressed and were finally abolished by treatment with a CaM inhibitor chlorpromazine (1–100 μM) in a concentration-dependent manner. Another CaM antagonist calmidazolium (1 μM) showed a similar effect. In contrast, CaMKII inhibitors, KN-62 (0.1–3 μM) and autocamtide 2–related inhibitory peptide (1 μM), delayed the development of CDF and CDI significantly, but they did not depress either CDF or CDI. These results imply that CaM is necessary and possiblly sufficient for the two mechanisms. We propose a hypothesis that CaM is a key molecule to bifurcate the Ca2+ signal to CDF and CDI and that CaMKII plays a modulatory role in them both.
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  • Hiroko Kitaoka, Gary F. Nieman, Yuji Fujino, David Carney, Joseph DiRo ...
    2007 Volume 57 Issue 3 Pages 175-185
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: June 02, 2007
    JOURNAL FREE ACCESS
    The alveolar structure, a space-filling branching duct system with alveolar openings, is one of the most complicated structures in the living body. Although its deformation during ventilation is the basic knowledge for lung physiology, there has been no consensus on it because of technical difficulties of dynamic 3-dimensional observation in vivo. It is known that the alveolar duct wall (primary septa) in the fetal lung is deformed so as to obtain the largest inner space and the widest surface area, and that the secondary septa grow just before birth and their free ridges form the alveolar entrance rings (mouths) containing abundant elastin fibers. We have constructed a 4-dimensional alveolar model according to this morphogenetic process, where the alveolar deformation is modeled by a combination of springs and hinges, corresponding to elastin fibers at alveolar mouths and junctions of alveolar septa, respectively. The model includes a hypothesis that alveolar mouths are closed at minimum volume and that closed alveoli are stabilized by the alveolar lining liquid film containing a surfactant. Morphometric characteristics of the model were consistent with previous reports. Furthermore, the model explained how the alveolar number and size could change during ventilation. Using in vivo microscopy, we validated our model by an analysis of the dynamic inflation and deflation of subpleural alveoli. Our model, including the alveolar mouth-closure hypothesis, can explain the origin of phase IV in a single breath nitrogen washout curve (closing volume) and mechanism of alveolar recruitment/derecruitment.
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  • V. Nimet İzgüt-Uysal, Mehmet Bülbül, Ruken Tan, ...
    2007 Volume 57 Issue 3 Pages 187-192
    Published: 2007
    Released on J-STAGE: June 21, 2007
    Advance online publication: June 05, 2007
    JOURNAL FREE ACCESS
    Background and Aim: L-Carnitine is an essential cofactor in the mitochondrial transfer of fatty acids, and it is also a scavenger of free radicals in mammalian tissues. The aim of the study was to determine the effect of L-carnitine on chronic restraint stress–induced gastric mucosal injury. Methods: Wistar rats were applied restraint stress (1 h/day) and L-carnitine (50 mg/kg) for 21 days. The lesion index, prostaglandin E2 and mucus content, lipid peroxidation, superoxide dismutase, and catalase activity in gastric mucosa were evaluated. Results: Chronic restraint stress increased the lesion index, lipid peroxidation, and superoxide dismutase activity in gastric mucosa, and it decreased prostaglandin E2 and mucus content. L-Carnitine treatment prevented the stress-induced increase in lesion index, lipid peroxidation and a stress-induced decline in prostaglandin E2, and mucus content in gastric mucosa, but it increased catalase activity. Conclusions: L-Carnitine prevents the occurrence of lesion by strengthening the gastric mucosal barrier and by reducing lipid peroxidation against the harmful effects of chronic restraint stress.
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