The Japanese Journal of Physiology
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Volume 51, Issue 3
Displaying 1-15 of 15 articles from this issue
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REVEIWS
  • Brain Angiotensin and Body Fluid Homeostasis
    M. J. McKinley, A. M. Allen, M. L. Mathai, C. May, R. M. McAllen, B. J ...
    2001 Volume 51 Issue 3 Pages 281-289
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.281
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    Angiotensinogen, the precursor molecule of the peptides angiotensin I, II, and III, is synthesized in the brain and the liver. Evidence is reviewed that angiotensin II, and possibly angiotensin III, that are generated within the brain act within neural circuits of the central nervous system to regulate body fluid balance. Immunohistochemical studies in the rat brain have provided evidence of angiotensin-containing neurons, especially in the hypothalamic paraventricular nucleus, subfornical organ, periventricular region, and nucleus of the solitary tract, as well as in extensive angiotensin-containing fiber pathways. Angiotensin immunoreactivity is observed by electron microscope in synaptic vesicles in several brain regions, the most prominent of these being the central nucleus of the amygdala. Neurons in many parts of the brain (lamina terminalis, paraventricular and parabrachial nuclei, ventrolateral medulla, and nucleus of the solitary tract) known to be involved in the regulation of body fluid homeostasis exhibit angiotensin receptors of the AT1 subtype. Pharmacological studies in several species show that intracerebroventricular administration of AT1 receptor antagonist drugs inhibit homeostatic responses to the central administration of hypertonic saline, intravenous infusion of the hormone relaxin, or thermal dehydration. Responses affected by centrally administered AT1 antagonists are water drinking, vasopressin secretion, natriuresis, increased arterial pressure, reduced renal renin release, salt hunger, and thermoregulatory adjustments. We conclude that angiotensinergic neural pathways in the brain probably have an important homeostatic function, especially in regard to osmoregulation and thermoregulation, and the maintenance of arterial pressure.
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  • Selective Brain Cooling in Mammals and Birds
    Claus Jessen
    2001 Volume 51 Issue 3 Pages 291-301
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.291
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    Artiodactyls and felids have a carotid rete that can cool the blood destined for the brain and consequently the brain itself if the cavernous sinus receives cool blood returning from the nose. This condition is usually fulfilled in resting and moderately hyperthermic animals. During severe exercise hyperthermia, however, the venous return from the nose bypasses the cavernous sinus so that brain cooling is suppressed. This is irreconcilable with the assumption that the purpose of selective brain cooling (SBC) is to protect the brain from thermal damage. Alternatively, SBC is seen as a mechanism engaging the thermoregulatory system in a water-saving economy mode in which evaporative heat loss is inhibited by the effects of SBC on brain temperature sensors. In nonhuman mammals that do not have a carotid rete, no evidence exists of whole-brain cooling. However, the surface of the cavernous sinus is in close contact with the base of the brain and is the likely source of unregulated regional cooling of the rostral brain stem in some species. In humans, the cortical regions next to the inner surface of the cranium are very likely to receive some regional cooling via the scalp-sinus pathway, and the rostral base of the brain can be cooled by conduction to the nearby respiratory tract; mechanisms capable of cooling the brain as a whole have not been found. Studies using conventional laboratory techniques suggest that SBC exists in birds and is determined by the physical conditions of heat transfer from the head to the environment instead of physiological control mechanisms. Thus except for species possessing a carotid rete, neither a coherent pattern of SBC nor a unifying concept of its biological significance in mammals and birds has evolved.
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Regular Papers
  • Lactate Release, Concentration in Blood, and Apparent Distribution Volume after Intense Bicycling
    Jon Ingulf Medbø, Karin Toska
    2001 Volume 51 Issue 3 Pages 303-312
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.303
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    To study the release of lactate from muscle and its relationship to the blood lactate concentration during and after intense bicycling, young men cycled at 5.5 W kg−1 body mass for 2 min to exhaustion or stopped after 1 min (nonexhaustive ride). The leg's release of lactate during and after each ride was taken from the measured blood flow and lactate concentrations in arterial and femoral-venous blood. Muscle biopsies were taken in separate experiments and analyzed for lactate. During the bicycling, 6 to 10% of the lactate produced was released to the blood. During exercise and for the first few minutes after, the rate of lactate release did not differ between 2 min exhaustive and 1 min nonexhaustive bicycling. The integrated release (exercise plus recovery) for the 1 min bicycling was 60 to 80% of the corresponding value of the 2 min exhaustive bicycling. In the late recovery, the blood lactate concentration was 3 to 5 times higher after 2 min exhaustive bicycling than after the 1 min nonexhaustive bicycling. There was thus a mismatch between the amount of lactate released and measured concentration in blood, reflecting a smaller distribution volume after the exhaustive bicycling. The blood lactate concentration may therefore not be a good measure of the lactate production and anaerobic energy release during bicycling.
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  • Expression of Vascular Endothelial Growth Factor and Its Receptors in the Developing Rat Lung
    Andrzej Marszalek, Tsutomu Daa, Kenji Kashima, Iwao Nakayama, Shigeo Y ...
    2001 Volume 51 Issue 3 Pages 313-318
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.313
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    We examined the regulation of the expression of vascular endothelial growth factor (VEGF) and its specific receptors, fetal liver kinase receptor (Flk-1), and fms-like tyrosine kinase receptor (Flt-1) during formation of the capillary network in the developing rat lung. An immunohistochemical study of lung tissue from 19- and 21-d-old fetuses and 1-, 3-, 5-, 7-, and 14-d-old animals revealed that the level of expression of both VEGF and Flk-1 is significantly higher before birth (p < 0.0001) than after. Increased expression of Flt-1 on the first day after birth (p < 0.0001) suggests that this receptor might play an important role in capillary growth in the perinatal period. Immunostaining also revealed the colocalization of VEGF, Flt-1, and Flk-1 in endothelial cells of the lung capillaries at the ultrastructural level. The present studies revealed that VEGF and its two receptors are upregulated during the development of capillaries in the fetal and newborn rat lung.
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  • Cross-Bridge and Calcium Behavior in Ferret Papillary Muscle in Different Thyroid States
    Naoto Yagi, Yasutake Saeki, Tetsuya Ishikawa, Satoshi Kurihara
    2001 Volume 51 Issue 3 Pages 319-326
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.319
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    X-ray diffraction studies were made using synchrotron radiation on ferret right ventricular papillary muscle under three different thyroid states: euthyroidism, hyperthyroidism, and hypothyroidism. The latter two states were induced by treatment with L-thyroxine and methimazole, respectively. The X-ray equatorial reflections were recorded at a time resolution of 10 ms to study the mass movement of myosin cross-bridges from thick to thin filaments. The myosin isomer content was measured by gel electrophoresis which showed that V3 isomer was predominant in euthyroid muscle and 27% of myosin was V1 isomer in hyperthyroid muscle. The intracellular free Ca concentration was measured by using the aequorin method. The peak Ca concentration was similar in all three states, but in the hypothyroid state the time-to-peak was longer and the decay was slower. The time-to-peak of twitch tension was shorter in hyperthyroidism and longer in hypothyroidism than in euthyroidism. The different time courses of twitch tension in different thyroid states accompanied a cross-bridge movement which closely followed the tension development. In hyperthyroidism, the cross-bridge movement significantly preceded tension development, suggesting that hyperthyroid myosin (V1) has a longer latency period between the shift to the vicinity of the thin filament and force development.
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  • Involvement of Different Activator Ca2+ in the Rate-Dependent Stretch-Induced Contractions of Canine Basilar Artery
    Kazuo Obara, Michihiro Saito, Akihiro Yamanaka, Mayumi Uchino, Koichi ...
    2001 Volume 51 Issue 3 Pages 327-335
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.327
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    Stretch evoked a contraction in a rate-dependent manner in canine basilar artery; slow stretch at rates less than 3 mm/s produced no active tension, whereas quick stretch at rates over 5 mm/s did. Large conductance Ca2+-activated K+ channel blockers, including charybdotoxin, iberiotoxin, and tetraethylammonium (TEA) sensitized the basilar artery to mechanical stimulation. TEA shifted the stretch rate-tension relationship toward the left. Thus, in the presence of TEA, the slow stretch (0.1-3 mm/s) could increase in intracellular Ca2+ concentration ([Ca2+]i) and active tension. The contraction in response to slow stretch (1 mm/s) was abolished by nicardipine and Gd3+. Quick stretch (100 mm/s) increased [Ca2+]i and active tension, both of which were partially inhibited by nicardipine or Gd3+. The Gd3+-insensitive component of quick stretch-induced contraction was eliminated by thapsigargin, but not by nicardipine. Ryanodine, cyclopiazonic acid, thapsigargin, U-73122, and calphostin C also abolished the nicardipine-insensitive component of quick stretch-induced contraction. These results suggest that the slow stretch-induced contraction was exclusively dependent on the Ca2+ influx through L-type voltage-dependent Ca2+ channels (VDCs), whereas the quick stretch-induced contraction was dependent on Ca2+ release from sarcoplasmic reticulum (SR) and Ca2+ influx through L-type VDCs.
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  • Roles of α1 and α1/β Subunits Derived from Cardiac L-Type Ca2+ Channels on Voltage-Dependent Facilitation Mechanisms
    Tae-Seong Lee, Katsushige Ono, Tetsuo Hadama, Yuzo Uchida, Makoto Arit ...
    2001 Volume 51 Issue 3 Pages 337-344
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.337
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    Strong depolarization pulses facilitate L-type Ca2+ channels in various cell types including cardiac myocytes. The mechanisms underlying prepulse facilitation are controversial with respect to the requirements for channel subunits, cAMP-dependent protein kinase, and additional anchor proteins. The properties of voltage-dependent facilitation of the L-type Ca2+ channel was studied in recombinant cardiac α1 subunits with or without cardiac β subunit, expressed in Chinese hamster fibroblast cells. The magnitude of voltage-dependent IBa facilitation in the α1 subunit channel is dependent on the duration of the prepulse as well as on the interval duration between prepulse and test pulse. The characteristics of this facilitation were not affected by coexpression of the β subunit. These results indicate that cardiac α1 subunits exhibit voltage-dependent facilitation because of their own intrinsic structure, independent of any other accessory subunit or additional regulatory proteins, and that cardiac β subunits have no essential regulatory role at the onset or continuance of the voltage-dependent facilitation.
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  • A Voltage-Dependent Transient K+ Current in Rat Dental Pulp Cells
    Yoshiyuki Shibukawa, Takashi Suzuki
    2001 Volume 51 Issue 3 Pages 345-353
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.345
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    We characterized a voltage-dependent transient K+ current in dental pulp fibroblasts on dental pulp slice preparations by using a nystatin perforated-patch recording configuration. The mean resting membrane potential of dental pulp fibroblasts was −53 mV. Depolarizing voltage steps to +60 mV from a holding potential of −80 mV evoked transient outward currents that are activated rapidly and subsequently inactivated during pulses. The activation threshold of the transient outward current was −40 mV. The reversal potential of the current closely followed the K+ equilibrium potential, indicating that the current was selective for K+. The steady-state inactivation of the peak outward K+ currents described by a Boltzmann function with half-inactivation occurred at −47 mV. The K+ current exhibited rapid activation, and the time to peak amplitude of the current was dependent on the membrane potentials. The inactivation process of the current was well fitted with a single exponential function, and the current exhibited slow inactivating kinetics (the time constants of decay ranged from 353 ms at −20 mV to 217 ms at +60 mV). The K+ current was sensitive to intracellular Cs+ and to extracellular 4-aminopyridine in a concentration-dependent manner, but it was not sensitive to tetraethylammonium, mast cell degranulating peptide, and dendrotoxin-I. The blood depressing substance-I failed to block the K+ current. These results indicated that dental pulp fibroblasts expressed a slow-inactivating transient K+ current.
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  • A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells
    Manabu Yanagisawa, Kazuo Suzuki
    2001 Volume 51 Issue 3 Pages 355-363
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.355
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    The effects of islet hormones, insulin and somatostatin, on the regulation of the opening of Ca2+-activated K+ channels in the basolateral plasma membrane of primary cultured pancreatic acinar cells of guinea-pig were studied by cell-attached single-channel recording technique. A single application of insulin or somatostatin did not influence the opening of K+ channel. The open-state probability (p) of K+ channel induced by the application of acetylcholine (ACh) to the bath solution was increased by insulin in the presence of ACh. The enhancement effect of insulin on the increased frequency of the channel opening was not seen when concomitantly applied with protein kinase A inhibitor, Rp-cAMPS triethylamine. Insulin increased the p value of K+ channel, which was reversed by an application of somatostatin (Tyr-somatostatin 28). The addition of ACh followed by forskolin or dibutyryl adenosine 3′,5′-cyclic monophosphate (dbcAMP) to the bath solution evoked an increase in the p value of K+ channel. After increasing the channel opening, the addition of somatostatin reduced the p value, but not with dbcAMP. Taken together, the results suggest that insulin and somatostatin reciprocally modify the ACh-induced opening of the Ca2+-activated K+ channel through a cyclic AMP-dependent signaling pathway.
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  • Laterality in Direct and Indirect Inotropic Effects of Sympathetic Stimulation in Isolated Canine Heart
    Yasunori Nakayama, Hiroshi Miyano, Toshiaki Shishido, Masashi Inagaki, ...
    2001 Volume 51 Issue 3 Pages 365-370
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.365
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    Although sympathetic nerve stimulation is known to increase ventricular contractility, concomitant increases in heart rate (HR) make it difficult to separate its direct inotropic effect from indirect inotropic effect through a force-frequency mechanism. We stimulated the stellate ganglia in 8 isolated canine hearts with functional sympathetic nerves. Right sympathetic stimulation at 10 Hz increased ventricular end-systolic elastance (Ees) by 95.7 ± 7.5% (p < 0.001) and HR by 32.5 ± 4.2% (p < 0.05). In contrast, left sympathetic stimulation at 10 Hz increased Ees by 70.7 ± 6.5% (p < 0.001) without significant changes in HR. Preventing the chronotropic response by fixed-rate pacing attenuated the Ees response to right sympathetic stimulation at 5 Hz (52.0 ± 5.1 vs. 22.8 ± 2.8%, p < 0.001), but not to left sympathetic stimulation at 5 Hz (54.5 ± 3.4 vs. 53.3 ± 2.2%, NS). In the isolated canine heart, the right sympathetic nerve affected Ees by both the direct inotropic effect and the indirect HR-dependent inotropic effect. In contrast, the left sympathetic nerve regulated Ees primarily by its direct inotropic effect.
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  • Ca2+-Dependent Inhibition of Inwardly Rectifying K+ Channel in Opossum Kidney Cells
    Yoshiaki Mori, Atsushi Kawasaki, Atsuko Takamaki, Ikuo Kitano, Ryotaro ...
    2001 Volume 51 Issue 3 Pages 371-380
    Published: 2001
    Released on J-STAGE: June 19, 2004
    DOIhttps://doi.org/10.2170/jjphysiol.51.371
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    The effect of intracellular Ca2+ on the activity of the inwardly rectifying ATP-regulated K+ channel with an inward conductance of about 90 pS was examined by using the patch-clamp technique in opossum kidney proximal tubule (OKP) cells. The activity of the inwardly rectifying K+ channel rapidly declined with an application of ionomycin (1 μM) in the presence of 10−6 M Ca2+ in cell-attached patches. The application of 10 μM phorbor-12-myristate-acetate (PMA) with 10−6 M Ca2+ reduced the K+ channel activity. Although the channel activity was not influenced by an increase of bath Ca2+ from 10−7.5 to 10−6 M, the activity was inhibited by protein kinase C (PKC, 1 U/ml) with 10−6 M Ca2+ in inside-out patches. The inhibitory effect of Ca2+ with ionomycin on the channel activity was diminished by the pretreatment with a specific PKC inhibitor, GF 109203X (5 μM), in cell-attached patches. By contrast, the application of Ca2+/calmodulin kinase II (CaMK II, 300 pM) dramatically increased this channel activity in inside-out patches. In cell-attached patches, the addition of both GF 109203X and cyclospolin A (5 μM), a potent inhibitor of protein phosphatase 2B (calcineurin), instead stimulated the K+ channel activity with ionomycin and 10−6 M Ca2+. The addition of protein phosphatase 2B (calcineurin) (2 U/ml) to the bath with calmodulin (1 μM) and Ni2+ (10 μM) to stimulate calcineurin inhibited the channel activity in inside-out patches. Furthermore, the inhibitory effect of PKC or calcineurin on this channel activity was abolished by a removal of Ca2+ from bath solution. These results suggest that Ca2+-dependent inhibitory effect on the inwardly rectifying K+ channel in OKP cells was mainly mediated by Ca2+-PKC-mediated phosphorylation, and that the Ca2+-calmodulin-dependent phosphorylation process may be counterbalanced by the Ca2+-calmodulin-dependent dephosphorylation process.
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