• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.231-241
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• 2001

The mammalian cortical collecting duct (CCD) plays a major role in regulating renal NaCl reabsorption, which is important in $Na^+$ and $Cl^-$ homeostasis. The M-1 cell line, derived from the mouse cortical collecting duct, has been used as a mammalian model of the study on the electrolytes transport in CCD. M-1 cells were grown on collagen-coated permeable support and short circuit current $(I_{sc})$ was measured. M-1 cells developed amiloride-sensitive current $5{\sim}7$ days after seeding. Apical and basolateral addition of ATP induced increase in $I_{sc}$ in M-1 cells, which was partly retained in $Na^+-free$ or $Cl^--free$ solution, indicating that ATP increased $Na^+$ absorption and $Cl^-$ secretion in M-1 cells. $Cl^-$ secretion was mediated by the activation of apical cystic fibrosis transmembrane regulator (CFTR) chloride channels and $Ca^{2+}-activated$ chloride channels, but $Na^+$ absorption was not mediated by activation of epithelal sodium channel (ENaC). ATP increased cAMP content in M-1 cells. The RT-PCR analysis demonstrated that M-1 cells express $P2Y_2,\;P2X_3\;and\;P2Y_4$ receptors. These results showed that ATP regulates $Na^+$ and $Cl^-$ transports via multiple P2 purinoceptors on the apical and basolateral membranes in M-1 cells.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.225-232
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• 1998

To investigate the possible involvement of outward potassium ($K^+$) currents in nitric oxide-induced relaxation in intestinal smooth muscle, we used whole-cell patch clamp technique in freshly dispersed guinea-pig ileum longitudinal smooth muscle cells. When cells were held at -60 mV and depolarized from -40 mV to -50 mV in 10 mV increments, sustained outward $K^+$ currents were evoked. The outward $K^+$ currents were markedly increased by the addition of 10 ${\mu}M$ sodium nitroprusside (SNP). 10 ${\mu}M$ S-nitroso-N-acetylpenicillamine (SNAP) and 1 mM 8-Bromo-cyclic GMP (8-Br-cGMP) also showed a similar effect to that of SNP. 1 mM tetraethylammonium (TEA) significantly reduced depolarization-activated outward $K^+$ currents. SNP-enhanced outward $K^+$ currents were blocked by the application of TEA. High EGTA containing pipette solution (10 mM) reduced the control currents and also inhibited the SNP-enhanced outward $K^+$ currents. 5 mM 4-aminopyridine (4-AP) significantly reduced the control currents but showed no effect on SNP-enhanced outward $K^+$ currents. 0.3 ${\mu}M$ apamin and 10 ${\mu}M$ glibenclamide showed no effect on SNP-enhanced outward $K^+$ currents. 10 ${\mu}M$ 1H-[1,2,4]oxadiazolo [4,3-a]quinoxaline-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase, significantly blocked SNP-enhanced $K^+$ currents. We conclude that NO donors activate the $Ca^{2+}-activated$ $K^+$ channels in guinea-pig ileal smooth muscle via activation of guanylate cyclase.

• The Korean Journal of Zoology
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• v.28 no.4
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• pp.227-236
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• 1985

In an attempt to make a scrutiny into a mechanism for the formation of quaternary structure of LDH isozymes, male mice were intraperitoneally exposed to a wide range of tetrodotoxin concentration and the changes in relative percentage of the five isozymes were monitored by electrophoresis and subsequent densitometry. The observations that a conspicuous increase of the $H_4$ isozyme was demonstrated in nearly all brain tissues, that the $M_4$ isozyme of skeletal muscle tissue was slightly increased while the $M_3H$ and $M_2H_2$ isozymes were decreased, that the M/H ratio was strikingly reduced in heart tissue and that assembly of $H_4$ isozyme was revealed in liver tissue although its rate was extremely low suggest that new intracellular ionic environment established by compulsory change in Donnan equilibrium could alter the LDH isozyme distribution. The reduction of assembly of $M_3H$ isozyme found in mouse tissues exposed to tetrodotoxin also seems to suggest that the subunit combination of 3M+H is very unfavorable in an intracellular environment deviated from its accustomed one. It was reaffirmed that there might occur TTX-insensitive sodium channels in plasma membrane.

• Biomolecules & Therapeutics
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• v.8 no.1
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• pp.13-21
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• 2000

The present study was designed to investigate the effect f quinidine on catecholamine (CA) secretion evoked by ACh, high $K^{+}$, DMPP, McN-A343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of quinidine (15-150 $\mu$M) into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition in CA secretion evoked by ACh (5.32$\times$10$^{-3}$ M), high $K^{+}$ (5.6$\times$10$^{-2}$ M), DMPP (10$^{-4}$ M for 2 min), McN-A-343 (10$^{-4}$ M for 2 min), cyclopiazonic acid (10$^{-5}$ M for 4 min) and Bay-K-8644 (10$^{-5}$ M for 4 min). Furthermore, in adrenal glands pre-loaded with quinine (5$\times$10$^{-5}$ M), CA secretory responses evoked by veratridine (10$^{-4}$ M) was time-dependently inhibited. Also, in the presence of lidocaine (10$^{-4}$ M), which is also known to be a sodium channel blocker, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclo-piazonic acid were also greatly reduced in similar fashion to that of quinidine-treatment. Taken together, these results suggest that quinidine causes greatly the inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating strongly that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells. Furthermore, these findings indicate strongly that this inhibitory action of quinidine appears to be associated to the blocking action of sodium channels at least in CA secretion from the rat adrenal gland.and.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.3
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• pp.331-341
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• 2018

The aim of the present study was to examine the effects of preemptive analgesia on the development of trigeminal neuropathic pain. For this purpose, mechanical allodynia was evaluated in male Sprague-Dawley rats using chronic constriction injury of the infraorbital nerve (CCI-ION) and perineural application of 2% QX-314 to the infraorbital nerve. CCI-ION produced severe mechanical allodynia, which was maintained until postoperative day (POD) 30. An immediate single application of 2% QX-314 to the infraorbital nerve following CCI-ION significantly reduced neuropathic mechanical allodynia. Immediate double application of QX-314 produced a greater attenuation of mechanical allodynia than a single application of QX-314. Immediate double application of 2% QX-314 reduced the CCI-ION-induced upregulation of GFAP and p-p38 expression in the trigeminal ganglion. The upregulated p-p38 expression was co-localized with NeuN, a neuronal cell marker. We also investigated the role of voltage-gated sodium channels (Navs) in the antinociception produced by preemptive application of QX-314 through analysis of the changes in Nav expression in the trigeminal ganglion following CCI-ION. Preemptive application of QX-314 significantly reduced the upregulation of Nav1.3, 1.7, and 1.9 produced by CCI-ION. These results suggest that long-lasting blockade of the transmission of pain signaling inhibits the development of neuropathic pain through the regulation of Nav isoform expression in the trigeminal ganglion. Importantly, these results provide a potential preemptive therapeutic strategy for the treatment of neuropathic pain after nerve injury.

• The Korean Journal of Pain
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• v.34 no.3
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• pp.262-270
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• 2021

Background: Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel implicated in pain sensation in response to heat, protons, and capsaicin (CAPS). It is well established that TRPV1 is involved in mechanical allodynia. This study investigates the effect of Ononis spinosa (Fabaceae) in CAPS-induced mechanical allodynia and its mechanism of action. Methods: Mechanical allodynia was induced by the intraplantar (ipl) injection of 40 ㎍ CAPS into the left hind paw of male Wistar rats. Animals received an ipl injection of 100 ㎍ O. spinosa methanolic leaf extract or 2.5% diclofenac sodium 20 minutes before CAPS injection. Paw withdrawal threshold (PWT) was measured using von Frey filament 30, 90, and 150 minutes after CAPS injection. A molecular docking tool, AutoDock 4.2, was used to study the binding energies and intermolecular interactions between O. spinosa constituents and TRPV1 receptor. Results: The ipsilateral ipl injection of O. spinosa before CAPS injection increased PWT in rats at all time points. O. spinosa decreased mechanical allodynia by 5.35-fold compared to a 3.59-fold decrease produced by diclofenac sodium. The ipsilateral pretreatment with TRPV1 antagonist (300 ㎍ 4-[3-Chloro-2-pyridinyl]-N-[4-[1,1-dimethylethyl] phenyl]-1-piperazinecarboxamide [BCTC]) as well as the β2-adrenoreceptor antagonist (150 ㎍ butoxamine) attenuated the action of O. spinosa. Depending on molecular docking results, the activity of the extract could be attributed to the bindings of campesterol, stigmasterol, and ononin compounds to TRPV1. Conclusions: O. spinosa alleviated CAPS-induced mechanical allodynia through 2 mechanisms: the direct modulation of TRPV1 and the involvement of β2 adrenoreceptor signaling.

• International Area Studies Review
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• v.13 no.1
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• pp.417-444
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• 2009

In October 2005, the Russian government started an investigation if safeguard measures against the importation of Korean sodium cyanide products could be taken. With Russia being a non-WTO member country, the Korean side found themselves in different situation from previous negotiation cases with developed or WTO member countries. Although several elements of trade negotiation theories such as goal setting, bargaining power, and relationship could apply, new constraints of limited information access and uncertainty of administrative procedures should be overcome. Combination of the governmental negotiation, assistance of the Russian consumer group, and the application of related laws led the Russian authority to dismiss the case. I suggest that there be some built-in channels for gathering information of non-WTO member countries.

• The Korean Journal of Physiology
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• v.27 no.1
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• pp.57-66
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• 1993

Effects of a voltage dependent calcium channel antagonist, nifedipine, on the responses of blood pressure, and secretion of atrial natriuretic peptide (ANP) and aldosterone to angiotensin II (Ang II) were compared in male Wistar and spontaneously hypertensive rats (SHR). A low, control or high sodium diet (2, 10 or 25 mmol Na/100 g diet) was fed for 6 weeks from the age of 6 weeks. On the morning of the experiment catheters were inserted under ether anesthesia in the femoral artery for pressure recording and blood sampling, and in the femoral vein for drug infusion. Ang II was infused at a rate of 250 ng/kg/min for 20 min. Nifedipine mixed with Ang II was infused at a rate of $16{\mu}g/kg/min$ for 20 min. Arterial blood samples were collected before and after infusion of Ang II with or without nifedipine. The control plasma level of aldosterone was inversely related to the amount of salt intake, whereas the plasma ANP level was not different between the salt groups. SHR showed a higher basal plasma ANP but a lower aldosterone concentration than Wistar rats. Infusion of Ang II produced a significant increase in blood pressure and plasma levels of aldosterone and ANP: The % increase was not significantly different either between the salt groups or between SHR and Wistar rats. SHR showed a greater pressor response to Ang II but a remarkably smaller decrease in heart rate after Ang II infusion than Wistar rats, With increasing sodium intake, the effect of Ang II on aldosterone secretion was decreased, whereas that on ANP secretion or blood pressure was not changed. Nifedipine decreased the responses of blood pressure and heart rate to Ang II in all groups. Nifedipine caused almost a complete inhibition of Ang II induced ANP secretion, but only a partial inhibition of Ang II induced aldosterone secretion or vasoconstriction. These results indicate that calcium dependent processes were involved in Ang II induced vasoconstriction, and secretions of aldosterone and ANP. However, the calcium dependent process far ANP secretion was considerably different from that for aldosterone secretion or vasoconstriction evoked by ang II. The ang II induced increase in ANP secretion appeared to be caused primarily by activating voltage-dependent calcium channels, whereas Ang II induced aldosterone secretion and vasoconstriction was not.

• Journal of Applied Biological Chemistry
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• v.44 no.3
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• pp.105-112
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• 2001

Insect pests can be controlled through direct application of insecticides. Insect control by residual protectants is relatively inexpensive and has an advantage of destroying all stages of infestations. The efficacy of control is largely determined by the concentration of insecticides to which the pest species is exposed. A reduction in the period of control in the field afforded by a specific level of a protectant indicates that resistance has developed. An increase in the level of protectant is required to maintain control, and the efficacy of currently used insecticides has been severely reduced by insecticide resistance in pest species. Development of resistance to particular insecticide varies with species because insecticide resistance is often correlated with increased levels of certain enzymes, which are cytochrome P450-dependent monooxygenases, glutathione S-transferases and esterases. Some sections of insecticide molecules can be modified by one or more of these primary enzymes. A reduction in the sensitivity of the action site of a xenobiotic also constitutes a mechanism of resistance. Acetylcholinesterase is a major target site for insecticide action, as are axonal sodium ion channels and ${\gamma}$-aminobutyric acid receptors. Development of reduced sensitivity of these target sites to insecticides usually occurs. This review not only may contribute to a better understanding of insecticide resistance, but also illustrates the gaps still present for a full biochemical understanding of the resistance.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.349-362
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• 2020

Temperature affects the firing pattern and electrical activity of neurons in animals, eliciting diverse responses depending on neuronal cell type. However, the mechanisms underlying such diverse responses are not well understood. In the present study, we performed in vitro recording of abdominal ganglia cells of Aplysia juliana, and analyzed their burst firing patterns. We identified atypical bursting patterns dependent on temperature that were totally different from classical bursting patterns observed in R15 neurons of A. juliana. We classified these abnormal bursting patterns into type 1 and type 2; type 1 abnormal single bursts are composed of two kinds of spikes with a long interspike interval (ISI) followed by short ISI regular firing, while type 2 abnormal single bursts are composed of complex multiplets. To investigate the mechanism underlying the temperature dependence of abnormal bursting, we employed simulations using a modified Plant model and determined that the temperature dependence of type 2 abnormal bursting is related to temperature-dependent scaling factors and activation or inactivation of potassium or sodium channels.