• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.1
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• pp.1-7
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• 2006

The present study was aimed to explore the role of sympathetic and parasympathetic nerves in the regulation of sodium transporters and water channels in the salivary gland. Rats were denervated of their sympathetic and parasympathetic nerves to the submandibular gland, and the glandular expression of sodium transporters and water channels was determined by Western blot analysis. The expression of either ${\alpha}1$ or ${\beta}1$ subunit of Na, K-ATPase was not significantly affected either by the sympathetic or by the parasympathetic denervation. The expression of subunits of epithelial sodium channels was significantly increased both in the denervated and contralateral glands either by the sympathetic or by the parasympathetic denervation. Neither the sympathetic nor the parasympathetic denervation significantly altered the expression of aquaporin-1 (AQP1). Nor was the expression of AQP4 affected significantly by the parasympathetic or the sympathetic denervation. On the contrary, the expression of AQP5 was significantly increased not only by the parasympathetic but also by the sympathetic denervation. These results suggest that sympathetic and parasympathetic nerves have tonic regulatory effects on the regulation of certain sodium transporters and AQP water channels in the salivary gland.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.65-69
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• 2006

The present study was undertaken to explore the role of autonomic nerves in the regulation of sodium transporters and water channels in the salivary gland. Rats were denervated of their sympathetic or parasympathetic nerves to the submandibular gland. One week later, the expression of Na,K-ATPase, epithelial sodium channels (ENaC), and aquaporins (AQP) was examined in the denervated and contralateral glands. The sympathetic denervation slightly but significantly decreased the expression of ${\alpha}1$ subunit of Na,K-ATPase, whereas the parasympathetic denervation increased it. The expression of ${\alpha}$-subunit of ENaC was significantly increased in both the denervated and contralateral glands either by the sympathetic or parasympathetic denervation. The sympathetic denervation significantly increased the expression of AQP5 in both the denervated and contralateral glands, whereas the parasympathetic denervation decreased it. It is suggested that the autonomic nerves have a tonic effect on the regulation of sodium transporters and AQP water channels in the salivary gland.

• Korean journal of applied entomology
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• v.61 no.1
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• pp.117-128
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• 2022

In this study, we have examined pyrethroid actions on sodium channels in the pest insect Heliothis virescens. The synthetic pyrethroid permethrin increased steady-state sodium current in H. virescens central neurons and prolonged tail currents (I_Na-tail) due to extreme slowing of sodium channel deactivation. Prolongation of I_Na-tail was evident at permethrin concentrations as low as 60 nM, which modified ~1.7% of sodium channels and 10 μM permethrin modified about 30% of channels. The average time constant (τ₁) of tail current decay was ~335 ms for permethrin-modified channels. These modified channels activated at more negative potentials and showed slower activation kinetics, and failed to inactivate. Permethrin modification of sodium channels was dramatically potentiated by the α scorpion toxin LqhαIT, showing positive cooperativity between two binding sites. The amplitude of the tail current induced by 0.3 μM permethrin was enhanced ~8-fold by LqhαIT (200 pM). Positive cooperativity was also observed between permethrin and the insect-specific scorpion toxin AaIT as 10 nM permethrin potentiated the shift of voltage dependence caused by AaIT (~2-fold).

• Journal of Life Science
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• v.2 no.2
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• pp.97-107
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• 1992

Strichartz and Richie have suggested that the mechanism of sodium donductance block of local anesthetics involves their interaction with a specific binding site within the sodium channel. However, there is evidence that local anesthetics can interact electrostatically with membrane proteins as well as membrane lipids. Whether or not all actions of local anesthetics are mediated by common site remains unclear. Thus, it can not be ruled out that local anesthetics concurrently interact with neuronal membrane lipids since sodium channels were found to be tightly associated with membrane lipids through covalent or noncovalent bonds. In summary, it is strongly postulated that local anesthetics, in addition to their direct interaction with sodium channels, concurrently interact with membrane lipids, fluidize the membrane, and thus induce conformational changes of sodium channels, which are known to be tightly associated with membrane lipids.

• Journal of Biomedical Engineering Research
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• v.2 no.2
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• pp.151-158
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• 1981

A modification of the Hodgkin-Huxley equations was done with the changes of the binding sitea for the sodium and potassium channels. The computer simulation results agree well with the currant experiments. Thus, the contradictory problems that Suh had indicated previously can be solved. And also, the results show that the sodium and potassium channels play an important role in the firing and the leakage channel does not.

• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.4
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• pp.305-312
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• 2015

Paeonol is a major component found in the Paeoniaceae family such as Paeonia suffruticosa Andrews. Paeonia suffruticosa Andrews has traditionally been used to enhance blood flow and relieve joint pain in east Asian countries including China, Korea and Japan. Current research has shown that paeonol blocked the voltage-gated sodium channel and L-type calcium channel. However, there is a lack of research to reveal the relation between cardiac function and blockade of ion channels by paeonol. Therefore, the aim of this study is to investigate whether paeonol has anti-arrhythmic effects via modulating cardiac ion channels. It is collected that the effects of paeonol on multiple ion channels such as the fast sodium channel and L-type calcium channel from published papers. To incorporate the information on multi-channel block, we computed the effects using the mathematical cardiac model of the guinea-pig and rat ventricular cells (Noble 1998 and 1991 model) and induced early after-depolarizations (EADs) to generate an arrhythmia in the whole heart. Paeonol slightly shortened the action potential duration in the normal cardiac ventricular action potential by the inhibition of sodium channel and L-type calcium channel. Paeonol presented the protective effect from EADs by the inactivation of sodium channel but not L-type calcium channel. Paeonol did not show any changes when it treated on normal ventricular cells through the inhibition of sodium channel, but the protective effect of paeonol through sodium channel on EADs was dose-dependent. These findings suggest that paeonol and its original plant may possess anti-arrhythmic activity, which implies their cardioprotective effects.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.1
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• pp.24-30
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• 2005

The flow of saliva is controlled entirely by nervous stimuli. The present study was aimed to explore the role of sympathetic and parasympathetic nerves in the regulation of sodium transporters and water channels in the salivary gland. Rats were denervated of their sympathetic and parasympathetic nerves to the submandibular gland, and the expression of sodium transporters and water channels was determined. The expression of either ${\alpha}-1$ or ${\beta}-1$ subunit of Na, K-ATPase was not significantly affected by the sympathetic denervation. On the contrary, the expression of both subunits was decreased by the parasympathetic denervation. The expression of ${\alpha}-,\;{\beta}-$, and ${\gamma}$-subunits of ENaC was not significantly affected by the sympathetic denervation, but was increased by the parasympathetic denervation. On the contrary, the expression of NHE3 was markedly decreased by both the sympathetic and the parasympathetic denervation. The sympathetic denervation significantly increased the expression of AQP1, while the parasympathetic denervation was without effect. The sympathetic and parasympathetic denervation significantly increased the expression of AQP4. The sympathetic denervation did not affect the expression of AQP5, but the parasympathetic denervation significantly decreased it. These results suggest that sympathetic and parasympathetic nerves have tonic effects on the regulation of sodium transporters and AQP water channels in the salivary gland. The sympathetic and parasympathetic denervation may then result in alterations of secretory rate and electrolyte composition of the saliva.

• Korean Chemical Engineering Research
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• v.54 no.6
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• pp.863-870
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• 2016

We investigated the physical/chemical phenomena that a slow loss of $CO_2$ inventory into sodium after the sodium-$CO_2$ boundary failure in printed circuit heat exchangers (PCHEs), which is considered for the supercritical $CO_2$ Brayton cycle power conversion system of a sodium-cooled fast reactor (SFR). The first phenomenon is plugging inside narrow sodium channels by micro cracks and the other one is damage propagation referred to as wastage combined with the corrosion/erosion effect. Experimental results of plugging shows that sodium flow immediately stopped as $CO_2$ was injected through the nozzle at $300{\sim}400^{\circ}C$ in 3 mmID sodium channels, whereas sodium flow stopped about 60 min after $CO_2$ injection in 5 mmID sodium channels. These results imply that if pressure boundary of sodium-$CO_2$ fails a narrow sodium channel would be plugged by reaction products in a short time whereas a relatively wider sodium channel would be plugged with higher concentration of reaction products. Wastage by the erosion effect of $CO_2$ (200~250 bar) hardly occurred regardless of the kinds of materials (stainless steel 316, Inconel 600, and 9Cr-1Mo steel), temperature ($400{\sim}500^{\circ}C$), or the diameter of the $CO_2$ nozzle (0.2~0.8 mm). Velocities at the $CO_2$ nozzle were specified as Mach 0.4~0.7. Our experimental results are expected to be used for determining the design parameters of PCHEs for their safeties.

• Biomolecules & Therapeutics
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• v.31 no.2
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• pp.168-175
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• 2023

Tramadol is an opioid analog used to treat chronic and acute pain. Intradermal injections of tramadol at hundreds of millimoles have been shown to produce a local anesthetic effect. We used the whole-cell patch-clamp technique in this study to investigate whether tramadol blocks the sodium current in HEK293 cells, which stably express the pain threshold sodium channel Na_v1.7 or the cardiac sodium channel Na_v1.5. The half-maximal inhibitory concentration of tramadol was 0.73 mM for Na_v1.7 and 0.43 mM for Na_v1.5 at a holding potential of -100 mV. The blocking effects of tramadol were completely reversible. Tramadol shifted the steady-state inactivation curves of Na_v1.7 and Na_v1.5 toward hyperpolarization. Tramadol also slowed the recovery rate from the inactivation of Na_v1.7 and Na_v1.5 and induced stronger use-dependent inhibition. Because the mean plasma concentration of tramadol upon oral administration is lower than its mean blocking concentration of sodium channels in this study, it is unlikely that tramadol in plasma will have an analgesic effect by blocking Na_v1.7 or show cardiotoxicity by blocking Na_v1.5. However, tramadol could act as a local anesthetic when used at a concentration of several hundred millimoles by intradermal injection and as an antiarrhythmic when injected intravenously at a similar dose, as does lidocaine.

• Clinical and Experimental Pediatrics
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• v.57 no.10
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• pp.445-450
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• 2014

Purpose: Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant channelopathy characterized by episodic attacks of muscle weakness and hypokalemia. Mutations in the calcium channel gene, CACNA1S, or the sodium channel gene, SCN4A, have been found to be responsible for HOKPP; however, the mechanism that causes hypokalemia remains to be determined. The aim of this study was to improve the understanding of this mechanism by investigating the expression of calcium-activated potassium ($K_{Ca}$) channel genes in HOKPP patients. Methods: We measured the intracellular calcium concentration with fura-2-acetoxymethyl ester in skeletal muscle cells of HOKPP patients and healthy individuals. We examined the mRNA and protein expression of KCa channel genes (KCNMA1, KCNN1, KCNN2, KCNN3, and KCNN4) in both cell types. Results: Patient cells exhibited higher cytosolic calcium levels than normal cells. Quantitative reverse transcription polymerase chain reaction analysis showed that the mRNA levels of the $K_{Ca}$ channel genes did not significantly differ between patient and normal cells. However, western blot analysis showed that protein levels of the KCNMA1 gene, which encodes $K_{Ca}$1.1 channels (also called big potassium channels), were significantly lower in the membrane fraction and higher in the cytosolic fraction of patient cells than normal cells. When patient cells were exposed to 50 mM potassium buffer, which was used to induce depolarization, the altered subcellular distribution of BK channels remained unchanged. Conclusion: These findings suggest a novel mechanism for the development of hypokalemia and paralysis in HOKPP and demonstrate a connection between disease-associated mutations in calcium/sodium channels and pathogenic changes in nonmutant potassium channels.