• Polymer(Korea)
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• v.25 no.5
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• pp.679-690
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• 2001

High resilience PU foams were prepared with polyether type cell opener. The influences of cell opener concentration on the kinetics, rheology, structural stability morphology and open cell content of the obtained foam were investigated and the role of cell opener during cell opening was determined. And mechanical properties as a function of cell opener concentration were studied. It was observed that urea formation reaction was delayed due to high hydrophilicity of cell opener The decrease of viscosity and the increase of tan $\delta$ were confirmed with increasing cell opener concentration so that the resulted foam had low structural stability and high open cell content. The deterioration of matrix and uniform dispersion of hydrogen-bonded urea in matrix with cell opener concentration was revealed by SEM analysis. As a result, elastic properties of the foam matrix were decreased due to high hydrophilicity of cell opener during the preparation of high resilience polyurethane foam and foam with high open cell content resulted. Hardness, tensile strength, tear strength, elongation of foam were decreased with increasing cell opener concentration.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.14 no.5
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• pp.2524-2528
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• 2013

Cell opening characteristics dependent on the cell openers for the conventional formulation of a closed-cell polyurethane foam (PUF) was studied using 1-butanol and lithium salt of 12-hydroxystearic acid (Li-12HSA) as the reactive cell opening agents. While cell openining content of only 10.5 % was obtained for the sample with 4 phr of 1-butanol as the single reactive cell opener, that of 98.0% could be obtained for the sample with 2 phr of Li-12HSA as the reactive co-cell opener. As the results, it showed that a fully open-cell rigid PUF could be obtained by introducing a novel reactive cell opener, having a functional group able to form a bulky side-chain on the urethane networks, without severe loss of mechanical properties of the closed-cell PUF like cell size, bulk density, and thermal conductivity.

• Polymer(Korea)
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• v.26 no.2
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• pp.218-226
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• 2002

For the preparation of high resilience polyurethane (PU) foams with polyether type cell openers which have different ethylene oxide (EO) content, molecular weight and chain structure, the influences of tell opener structure on the kinetics, rheology, structural stability, open cell content and mechanical properties of the obtained foam were investigated. It was observed that urea formation reaction was delayed with the increase of EO content and incorporation of ester linkage in cell opener molecule and was relatively independent on the molecular weight. With the rheological studies, the decreases of viscosity and storage modulus were confirmed for the increase of EO content and molecular weight, so that the resulted foam had low structural stability and high open cell content. The cell opener having ester linkage in molecule exhibited the lowest values of viscosity and storage modulus and the obtained foam has high open cell content. However, the structural stability increased due to the larger intermolecular interaction of ester linkage. The hardness, tensile strength, tear strength and elongation of foam were deteriorated with increase of EO content and molecular weight of tell opener. On the other hand, the cell opener having ester linkage in molecule improved the values of tensile strength, tear strength and elongation.

• Biomolecules & Therapeutics
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• v.9 no.2
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• pp.96-103
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• 2001

These studies were investigated about influence of SKP 450, a $K^{+}$ channel opener, on the pressor actions induced by norepinephrine, angiotensin II and carotid artery occlusion in rats. Before these studies, effect of SKP 450 itself on blood pressure was examinated. SKP 450 produced the depressor action in proportionaly to dose of 0.3, 1.0 and 3.0 $\mu$g/kg given intravenously and this depressor action was weakened by pretreatment of glibenclamide, a $K^{+}$ channel blocker. The pressor action induced by norepinephrine, an alpha-adrenergic agonist, was blocked 1 hr after administation of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v. and directly after in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The pressor action induced by angiotensin II was blocked immediatly after treatment of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v.. The pressor action caused by carotid artery occlusion was not affected by SKP 450 of 3.0 $\mu\textrm{g}$/kg, i.v., whereas markedly blocked by SKP 450 of 6.0 $\mu\textrm{g}$/㎦, i.v.. The potentiated-pressor actions of norepinephrine and angiotensin II by pretreatment of chlorisondamine, a autonomic ganglionic blocking agent, were also blocked by administration of SKP 450 in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The weakened-pressor action of carotid artery occlusion by pretreatment of chlorisondamine was more weakened by SKP 450 6.0 $\mu\textrm{g}$/kg, i.v.. The results suggest that hyperpolarization formed through $K^{+}$ channel opening in cell membrane inhibits the pressor action induced norepinephrine ; angiotensin II ; and carotid artery occlusion.usion.

• Archives of Pharmacal Research
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• v.28 no.12
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• pp.1358-1364
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• 2005

In this study, we investigated whether a novel anti-ischemic $K_{ATP}$ opener KR-31378 [(2S,3S,4R)­N'-cyano-N-(6-amino-3,4-dihydro-3-hydroxy-2 -methly-2-dimethoxymethly-2H-benzopyran-4-yl)­N'-benzylguanidine] has protective effect against oxidative stress-induced death in heart-derived H9c2 cells. Cell death was induced by BSO, butionine sulfoximine, which inhibits GSH synthesis and subsequently increases reactive oxygen species (ROS) level. Cell death was quantitatively determined by measuring lactate dehydrogenase (LDH) activity and stained by Hoechst 33258. BSO-induced ROS production and mitochondrial membrane potential (MMP) were measured using 2',7'-dichlorofluorescein diacetate oxidation and rhodamine 123, respectively. Both the LDH release and the ROS elevation induced by treatment of H9c2 cells with 10 mM BSO, were significantly decreased by KR-31378. These protective effect and antioxidant effect of KR-31378 appeared to be independent on $K_{ATP}$ channel opening. Cells exposed to BSO showed an early reduction in MMP, and this reduction in MMP was significantly reversed by treatment with KR-31378. Caspase-3 activity in BSO treated H9c2 cells was remarkably increased, and this increased caspase-3 activity was significantly reversed by KR-31378. In conclusion, our results suggest that KR-31378 can produce cardioprotective effect against oxidative stress-induced cell death through antioxidant mechanism.

• The Korean Journal of Physiology
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• v.28 no.1
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• pp.37-50
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• 1994

Synthetic potassium channel openers (KCOs) are agents capable of opening K-channels in excitable cells. These agents are known to have their maximal potency in the smooth muscle tissue, especially in the vascular smooth muscle. Much attention has been focused on the type of K-channel that is responsible for mediating the effects of KCOs. As the KCO-induced changes are antagonized by glibenclamide, an $K_{ATP}$ (ATP-sensitive K-channel) blocker in the pancreatic ${\beta}-cell,\;K_{ATP}$ was suggested to be the channel responsible. However, there also are many results in favor of other types of K-channel $$(maxi-K,\;small\;conductance\;K_{Ca,}\; SK_{ATP}) mediating the effects of KCOs. Effects of lemakalim, (-)enantiomer of cromakalim (BRL 34915), on the spontaneous contractions and slow waves, were investigated in the antral circular muscle of the guinea-pig stomach. Membrane currents and the effects on membrane currents and single channel activities were also measured in single smooth muscle cells and excised membrane patches by using the patch clamp method. Lemakalim induced hyperpolarization and inhibited spontaneous contractions in a dose-dependent manner. These effects were blocked by glibenclamide and low concentrations of tetraethyl ammonium (< mM). Glibenclamide blocked the effect of lemakalim on the membrane potential and slow waves. The mechanoinhibitory effect of lemakalim was blocked by pretreatment with glibenclamide. In a whole ceIl patch clamp condition, lemakalim largely increased outward K currents. These outward K currents were blocked by TEA, glibenclamide and a high concentration of intracelIular EGTA (10 mM). Volatage-gated Ca currents were not affected by lemakalim. In inside-out patch clamp experiments, lemakalim increased the opening frequency of the large conductance $Ca^{2+}-activated$ K channels $(BK_{Ca},\;Maxi-K).$ From these results, it is suggested that lemakalim induces hyperpolarization by opening K-channels which are sensitive to internal Ca and such a hyperpolarization leads to the inhibition of the spontaneous contraction.

• Journal of Life Science
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• v.29 no.12
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• pp.1393-1400
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• 2019

In the present study, we examined the effect of mitochondrial K⁺ channel opener diazoxide on the mitochondria-dependent apoptotic signaling in endothelial cells exposed to high glucose (HG) media. Endothelial cells derived from human umbilical veins were exposed to HG media containing 30 mM glucose, and the degree of apoptotic cell death associated with activation of the mitochondria-dependent apoptotic signaling pathway was determined. Exposure to HG media was seen to enhance apoptotic cell death in a time-dependent manner. In these cells, activation of caspases 3, 8, and 9 was observed, and while caspase-3 and -9 inhibitors suppressed the HG-induced apoptotic cell death, a caspase-8 inhibitor did not. The HG-treated cells exhibited disruption of mitochondrial membrane potential, formation of permeability transition pores, and cytosolic release of cytochrome c. Subsequently, diazoxide was seen to attenuate the HG-induced apoptotic cell death; caspase-9 activation was suppressed but caspase 8 was not. Diazoxide also suppressed the depolarization of mitochondrial membrane potential, the formation of mitochondrial permeability transition pores, and the release of cytochrome c. These effects were significantly inhibited by 5-hydroxydecanoate, a selective blocker of ATP-sensitive K⁺ channels (K_ATP). The present results demonstrate that diazoxide exhibits a beneficial effect to ameliorate HG-induced endothelial cell apoptosis. Opening the K_ATP could help preserve the functional integrity of mitochondria and provide an underlying mechanism to suppress HG-triggered apoptotic signaling.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.191-203
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• 1994

$K^+$ channel openers (KCOs) are known to have a wide range of effects by opening the $K^+$ channel in plasma membranes of various smooth muscles, cardiac muscle and pancreatic ${\beta}-cell$. In the present study, we investigated the effects of 5 types of KCOs, cromakalim, RP49356, pinacidil, nicorandil and diazoxide on the contractility of isolated rat uterus. All KCOs tested inhibited the uterine contraction induced by 0.2 nM oxytocin in a dose-dependent manner. Individual KCO and its $pD_2$ values were cromakalim 6.5, RP49356 6.3, pinacidil 5.92, nicorandil 4.43 and diazoxide 4.18. The relaxant effects of KCO were inhibited by glibenclamide (0.3, 1 and $10\;{\mu}M$) with $pA_2$ values of cromakalim 6.91, RP49356 6.59, pinacidil 6.55, nicorandil 5.97 and diazoxide 6.37. In addition, the relaxant effect of cromakalim or pinacidil was antagonised by TEA, a non-selective $K^+$ channel blocker, but not by apamin. Contractions induced by low concentration of KCI (< 40 mM) were inhibited by cromakalim $(100{\mu}M)$ and nicorandil $(300{\mu}M)$, but those evoked by higher concentration (> 40 mM) of KCI were little affected. In ovariectomized rat uterus, cromakalim dose-dependently inhibited oxytocin-induced contraction and glibenclamide $(10{\mu}M)$ inhibited the relaxant effect of cromakalim with $pD_2$ and $K_B$ values of 7.48 and $1.26{\times}10^{-7}M$, respectively. In estrogen-primed rat uterus, these values were 6.51 and $1.57{\times}10^{-7}M$, respectively, indicating that the cromakalim is less effective on the estrogen-treated uterine smooth muscle. Our results suggest that the KCO-sensitive $K^+$ channels participate in the motility of uterine smooth muscle and such channels are, at least in part, under the control of estrogen. In addition, our data Indicate that the type of $K^+$ channels activated by KCO is ATP-sensitive $K^+$ channels which is blocked by glibenclamide.