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The Korean journal of physiology & pharmacology : ... 15건

  1. [국내논문]   Aquaporins in the Kidney  

    Sasaki, Sei (Second Department of Internal Medicine, Tokyo Medical and Dental University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 271 - 277 , 1998 , 1226-4512 ,

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  2. [국내논문]   Effects of Glutamate Receptor Antagonists and Protein Synthesis Inhibitor on Delayed Neuronal Death Induced by Transient Global Ischemia in Rat Brain  

    Ko, Jun-Seog (Department of Pharmacology, Chonnam University Medical School and Chonnam University Research Institute of Medical Sciences ) , Bae, Choon-Sang (Department of Anatomy, Chonnam University Medical School and Chonnam University Research Institute of Medical Sciences ) , Kim, Jong-Keun (Department of Pharmacology, Chonnam University Medical School and Chonnam University Research Institute of Medical Sciences)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 279 - 286 , 1998 , 1226-4512 ,

    초록

    It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occured 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (1 mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

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  3. [국내논문]   Influence of the Central Benzodiazepinergic System on Peripheral Cardiovascular Regulation  

    Koh, Jeong-Tae (Departments of Pharmacology, Chonnam University College of Dentistry ) , Ju, Jeong-Min (Departments of Pharmacology, Chonnam University Medical School ) , Shin, Dong-Ho (Departments of Pharmacology, Chonnam University College of Veterinary Medicine ) , Cho, Han-Ho (Departments of Pharmacology, Chonnam University, Medical School ) , Choi, Bong-Kyu (College of Medicine, Wonkwang University ) , Kim, Jae-Ha (Departments of Pharmacology, Chonnam University Medical School)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 287 - 295 , 1998 , 1226-4512 ,

    초록

    Diazepam is known to have cardiovascular depressive effects through a combined action on benzodiazepinergic receptor and the GABA receptor-chloride ion channel complex. Moreover, it is known that barbiturates also have some cardiovascular regulatory effects mediated by the central GABAergic system. Therefore, this study was undertaken to delineate the regulatory actions and interactions of these systems by measuring the responses of the cardiovascular system and renal nerve activity to muscimol, diazepam and pentobarbital, administered intracerebroventricularly in rabbits. When muscimol $(0.03{\sim}0.3\;{\mu}\;g/kg)$ , diazepam $(10{\sim}100\;{\mu}\;g/kg)$ and pentobarbital $(1{\sim}10\;{\mu}\;g/kg)$ were injected into the lateral ventricle of the rabbit brain, there were similar dose-dependent decreases in blood pressure (BP) and renal nerve activity (RNA). The relative potency of the three drugs in decreasing BP and RNA was muscimol > pentobarbital > diazepam. Muscimol and pentobarbital also decreased the heart rate in a dose-dependent manner; however, diazepam produced a trivial, dose-independent decrease in heart rate. Diazepam $(30\;{\mu}g/kg)$ augmented the effect of muscimol $(0.1\;{\mu}g/kg)$ in decreasing blood pressure and renal nerve activity, but pentobarbital $(3\;{\mu}g/kg)$ did not. Bicuculline $(0.5\;{\mu}g/kg)$ , a GABAergic receptor blocker, significantly attenuated the effect of muscimol in decreasing BP and RNA, either alone or with diazepam, and that of pentobarbital in decreasing BP and RNA, either alone or with muscimol. We inferred that the central benzodiazepinergic and barbiturate systems help regulate peripheral cardiovascular function by modulating the GABAergic system, which adjusts the output of the vasomotor center and hence controls peripheral sympathetic tone. Benzodiazepines more readily modulate the GABAergic system than barbiturates.

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  4. [국내논문]   Characteristic Intracelluar Response to Lidocaine And MK-801 of Hippocampal Neurons: An In Vivo Intracellular Neuron Recording Study  

    Choi, Byung-Ju (Department of Dental Pharmacology, Kyungpook National University School of Dentistry ) , Cho, Jin-Hwa (Department of Dental Pharmacology, Kyungpook National University School of Dentistry)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 297 - 305 , 1998 , 1226-4512 ,

    초록

    This study used in vivo intracellular recording in rat hippocampus to evaluate the effect of lidocaine and MK-801 on the membrane properties and the synaptic responses of individual neurons to electrical stimulation of the commissural pathway. Cells in control group typically fired in a tonic discharge mode with an average firing frequency of $2.4{\pm}0.9$ Hz. Neuron in MK-801 treated group (0.2 mg/kg, i.p.) had an average input resistance of $3.28{\pm}5.7\;M{\Omega}$ and a membrane time constant of $7.4{\pm}1.8$ ms. These neurons exhibited $2.4{\pm}0.2$ ms spike durations, which were similar to the average spike duration recorded in the neurons of the control group. Slightly less than half of these neurons were firing spontaneously with an average discharge rate of $2.4{\pm}1.1$ Hz. The average peak amplitude of the AHP following the spikes in these groups was $7.4{\pm}0.6$ mV with respect to the resting membrane potential. Cells in MK-801 and lidocaine treated group (5 mg/kg, i.c.v.) had an average input resistance of $3.45{\pm}6.0\;M{\Omega}$ and an average time constant of $8.0{\pm}1.4$ ms. The cells were firing spontaneously at an average discharge rate of $0.6{\pm}0.4$ Hz. Upon depolarization of the membrane by 0.8 nA for 400 ms, all of the tested cells exhibited accommodation of spike discharge. The most common synaptic response contained an EPSP followed by early-IPSP and late-IPSP. Analysis of the voltage dependence revealed that the early-IPSP and late-IPSP were putative $Cl^--and\;K^+-dependent$ , respectively. Systemic injection of the NMDA receptor blocker, MK-801, did not block synaptic responses to the stimulation of the commissural pathway. No significant modifications of EPSP, early-IPSP, or late-IPSP components were detected in the MK-801 and/or lidocaine treated group. These results suggest that MK-801 and lidocaine manifest their CNS effects through firing pattern of hippocampal pyramidal cells and neural network pattern by changing the synaptic efficacy and cellular membrane properties.

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  5. [국내논문]   Intracisternal Antidepressants Suppressed the Nociceptive Jaw Opening Reflex in Freely Moving Rats  

    Ahn, Dong-Kuk (Department of Oral Physiology, School of Dentistry, Kyungpook National University ) , Kim, Yun-Sook (Department of Oral Physiology, School of Dentistry, Kyungpook National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 307 - 312 , 1998 , 1226-4512 ,

    초록

    This study was performed to investigate the mechanism of central analgesic effects of antidepressants. Thirty four male rats were anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula and a PE tube (PE10) were implanted into the lateral ventricle and cisterna magna area. Stimulating and recording electrodes were implanted into the incisor pulp and anterior digastric muscle. Electrodes were led subcutaneously to the miniature cranial connector sealed on the top of the skull with acrylic resin. The jaw opening reflex was used in freely moving rats, and antidepressants were administered intracisternally in order to eliminate the effects of anesthetic agents on the pain assessment and evaluate the importance of the central action site of antidepressants. After 48 hours of recovery from surgery, digastric electromyogram (dEMG) of freely moving rats was recorded. Electrical shocks (200 ${\mu}sec$ duration, 0.5-2 mA intensity) were delivered at 0.5 Hz to the dental pulp every 2 minute. Intracisternal administration of $15\;{\mu}g$ imipramine suppressed dEMG elicited by noxious electrical stimulation in the tooth pulp to $76{\pm}6%$ control. Intracisternal administration of $30\;{\mu}g$ desipramine, nortriptyline, or imipramine suppressed dEMG remarkably to $48{\pm}2,\;27{\pm}8,\;or\;25{\pm}5%$ of the control, respectively. Naloxone, methysergide, and phentolamine blocked the suppression of dEMG produced by intracisternal antidepressants from $23{\pm}2\;to\;69{\pm}4%,\;from\;32{\pm}5\;to\;80{\pm}9%,\;and\;from\;24{\pm}6\;to\;77{\pm}5%$ of the control, respectively. These results indicate that antidepressants produce antinociception through central mechanisms in the orofacial area. Antinociception of intracisternal antidepressants seems to be mediated by an augmentation of descending pain inhibitory influences on nociceptive pathways.

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  6. [국내논문]   Characteristics of $Ca^{2+}$ Stores in Rabbit Cerebral Artery Myocytes  

    Kim, Sung-Joon (Department of Physiology & Biophysics, Seoul National University College of Medicine ) , Kim, Jin-Kyung (Department of Anesthesiology, Seoul National University College of Medicine ) , So, In-Suk (Department of Physiology & Biophysics, Seoul National University College of Medicine ) , Suh, Suk-Hyo (Department of Physiology, Ewha Womans University College of Medicine ) , Lee, Sang-Jin (Department of Physiology, Chungbuk National University College of Medicine ) , Kim, Ki-Whan (Department of Physiology & Biophysics, Seoul National University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 313 - 322 , 1998 , 1226-4512 ,

    초록

    In a myocyte freshly isolated from rabbit cerebral artery, the characteristics of $Ca^{2+}$ release by histamine or caffeine were studied by microspectrofluorimetry using a $Ca^{2+}-binding$ fluorescent dye, fura-2. Histamine (5 ${\mu}M$ ) or caffeine (10 mM) induced a phasic rise of cytoplasmic free $Ca^{2+}$ concentration $([Ca^{2+}]_C)$ which could occur repetitively with extracellular $Ca^{2+}$ but only once or twice in $Ca^{2+}-free$ bathing solution. Also, the treatment with inhibitor of sarcoplasmic reticulum $Ca^{2+}-ATPase$ suppressed the rise of $[Ca^{2+}]_C$ by histamine or caffeine. In $Ca^{2+}-free$ bathing solution, short application of caffeine in advance markedly attenuated the effect of histamine, and vice versa. In normal $Ca^{2+}-containing$ solution with ryanodine (2 ${\mu}M$ ), the caffeine-induced rise of $[Ca^{2+}]_C$ occurred only once and in this condition, the response to histamine was also suppressed. On the other hand, in the presence of ryanodine, histamine could induce repetitive rise of $[Ca^{2+}]_C$ while the amplitude of peak rise became stepwisely decreased and eventually disappeared. These results suggest that two different $Ca^{2+}-release$ mechanisms (caffeine-sensitive and histamine-sensitive) are present in rabbit cerebral artery myocyte and the corresponding pools overlap each other functionally. Increase of $[Ca^{2+}]_C$ by histamine seems to partially activate ryanodine receptors present in caffeine-sensitive pool.

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  7. [국내논문]   Comparison of Inodilator Effect of Higenamine, YS49, YS51, Tetrahydroisoquinoline Analogs, and Dobutamine in the Rat  

    Chong, Won-Seog (Department of Pharmacology, Cardiovascular Research Institute, College of Medicine, Gyeongsang National University ) , Lee, Young-Soo (Department of Pharmacology, Cardiovascular Research Institute, College of Medicine, Gyeongsang National University ) , Kang, Young-Jin (Department of Pharmacology, Cardiovascular Research Institute, College of Medicine, Gyeongsang National University ) , Lee, Duck-Hyung (Department of Chemistry, Sogang University ) , Ryu, Jae-Chun (Doping Control Center, Korea Institute of Science and Technology ) , Yun-Choi, Hye-Sook (Natural Product Research Institute, Seoul National University ) , Chang, Ki-Churl (Department of Pharmacology, Cardiovascular Research Institute, College of Medicine, Gyeongsang National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 323 - 330 , 1998 , 1226-4512 ,

    초록

    Tetrahydroisoquinoline (THI) alkaloids can be considered as cyclized derivatives of simple phenylethylamines. Many of them, especially with 6,7-disubstitution, demonstrate a relatively high affinity for catecholamines. Present study examines the pharmacological action of limited series of THI, using rats' isolated atria and aorta. In addition, a $[^3H]$ prazosin displacement binding study with THI compounds was performed, using rat brain homogenates to investigate whether these probes have ? ${\alpha}$ -adrenoceptor affinity. We also compared the vascular relaxation potency of these probes with dobutamine. YS 49, YS 51, higenamine and dobutamine, concentration-dependently, relaxed endothelium-denuded rat thoracic aorta precontracted with phenylephrine (PE, 0.1 ${\mu}M$ ) in which $pEC_{50}$ were $5.56{\pm}0.32$ and $5.55{\pm}0.21$ , $5.99{\pm}1.16$ and $5.57{\pm}0.34$ , respectively. These probes except higenamine also relaxed KCl (65.4 mM)-contracted aorta. In isolated rat atria, all THIs and dobutamine increased heart rate and contractile force. In the presence of propranolol, the concentration response curves of YS 49 and YS 51 shifted to the right and resulted in $pA_2$ values of $8.07{\pm}0.84$ and $7.93{\pm}0.11$ , respectively. The slope of each compound was not deviated from unity, indicating that these chemicals are highly competitive at the cardiac ? ${\beta}-adrenoceptors$ . YS 49, YS 51, and higenamine showed ? ${\alpha)-adrenoceptor$ affinity in rat brain, in which the dissociation constant $(K_i)$ was 2.75, 2.81, and 1.02 ${\mu}M$ , respectively. It is concluded, therefore, that THI alkaloids have weak affinity to ${\alpha)_1-adrenoceptor$ in rat aorta and brain, respectively, while these probes show relatively high affinity for cardiac ${\beta}-adrenoceptors$ . Thus, these chemicals may be useful in the treatment of congestive heart failure.

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  8. [국내논문]   Cardioprotective Effects of Low Dose Bacterial Lipopolysaccharide May Not Be Directly Associated with Prostacyclin Production  

    Moon, Chang-Hyun (Department of Physiology, Scool of Medicine, Ajou University ) , Kim, Ji-Young (Department of Physiology, Scool of Medicine, Ajou University ) , Lee, Soo-Hwan (Department of Physiology, Scool of Medicine, Ajou University ) , Baik, Eun-Joo (Department of Physiology, Scool of Medicine, Ajou University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 331 - 343 , 1998 , 1226-4512 ,

    초록

    Sublethal dose of bacterial lipopolysaccharide (LPS) would induce protection against cardiac ischemic/reperfusion (I/R) injury. This study examines the following areas: 1) the temporal induction of the cardio-protection produced by LPS; and 2) the relations between a degree of protection and the myocardial prostacyclin ( $PGI_2$ ) production. Rats were administered LPS (2 mg/kg, i.v.), and hearts were removed 1, 4, 8, 14, 24, 48, 72,and 96 h later. Using Langendorff apparatus, haemodynamic differences during 25 min of global ischemia/30 min reperfusion were investigated. The concentration of $PGI_2$ in aliquots of the coronary effluent was determined by radioimmunoassay as its stable hydrolysis product $6-keto-PGF1_{\alpha}$ and lactate dehydrogenase release were measured as an indicative of cellular injury. LPS-induced cardiac protection against I/R injury appeared 4 h after LPS treatment and remained until 96 h after treatment. $PGI_2$ release increased 2-3 fold at the beginning of reperfusion compared to basal level except in hearts treated with LPS for 48 and 72 h. In hearts removed 48 and 72 h after LPS treatment, basal $PGI_2$ was increased. To determine the enzymatic step in relation to LPS-induced basal $PGI_2$ production, we examined prostaglandin H synthase (PGHS) protein expression, a rate limiting enzyme of prostaglandin production, by using Western blot analysis. LPS increased PGHS protein expression in hearts at 24, 48, 72, 96 h after LPS treatment. Induction of PGHS expression appeared in both isotypes of PGHS, a constitutive PGHS-1 and an inducible PGHS-2. To identify the correlationship between $PGI_2$ production and the cardioprotective effect against I/R injury, indomethacin was administered in vivo or in vitro. Indomethacin did not inhibit LPS-induced cardioprotection, which was not affected by the duration of LPS treatment. Taken together, our results suggest that $PGI_2$ might not be the major endogenous mediator of LPS-induced cardioprotection.

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  9. [국내논문]   Nitric Oxide Impairs the Recovery from Hemorrhagic Hypotension in Conscious Rats  

    Park, Yoon-Yub (Department of Physiology, School of Medicine, Catholic University of Taegu-Hyosung ) , Lee, Young-Man (Department of Physiology, School of Medicine, Catholic University of Taegu-Hyosung)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 345 - 351 , 1998 , 1226-4512 ,

    초록

    The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.

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  10. [국내논문]   Inhibitory Effect of Caffeine on Carbachol-Induced Nonselective Cationic Current in Guinea-Pig Gastric Myocytes  

    Kim, Sung-Joon (Heart Research Institute, Seoul National University Medical Research Center ) , Min, Kyung-Wan (Department of Physiology & Biophysics, Seoul National University College of Medicine ) , Kim, Young-Chul (Department of Physiology & Biophysics, Seoul National University College of Medicine ) , Lee, Sang-Jin (Department of Physiology, Chungbuk National University College of Medicine ) , So, In-Suk (Department of Physiology & Biophysics, Seoul National University College of Medicine ) , Kim, Ki-Whan (Department of Physiology & Biophysics, Seoul National University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.2 no.3 ,pp. 353 - 359 , 1998 , 1226-4512 ,

    초록

    In gastrointestinal smooth muscle, muscarinic stimulation by carbachol (CCh) activates nonselective cation channel current ( $I_{CCh}$ ) which is facilitated by intracellular [ $Ca^{2+}$ ] increase. Caffeine is widely used in experiments to mobilize $Ca^{2+}$ from intracellular stores. This study shows a strong inhibitory effect of caffeine on $I_{CCh}$ in guinea-pig gastric myocyte. In this study, the underlying mechanism of the inhibitory effect of caffeine was investigated. $I_{CCh}$ was completely suppressed by the addition of caffeine (10 mM) to the superfusing solution. Inhibition of $I_{CCh}$ by caffeine was not related to the intracellular cAMP accumulation which was expected from the phosphodiesterase-inhibiting effect of caffeine. The blockade of $InsP_3-induced$ $Ca^{2+}$ release by heparin had no significant effects on the activation of $I_{CCh}$ . When the same cationic current had been induced by intracellular dialysis of $GTP[{\gamma}S]$ in order to bypass the muscarinic receptor, the inhibitory effect of caffeine was significantly attenuated. The results of this study indicate that both intracellular signalling pathways for $I_{CCh}$ , proximal and distal to G-protein activation, are suppressed by caffeine. A major inhibition was observed at the proximal level.

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