• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.148-149
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• 1998

It has been known that potassium channel openers are a new class of molecules that have attracted general interest because of their potent antihypertensive activity in vivo and vasorelaxant activity in vitro (Hamilton and Weston, 1989). In the present study, it was attempted to examine the effect of the potassium channel opener on catecholamine (CA) secretion evoked by cholinergic stimulation, membrane depolarization and calcium mobilization from the isolated perfused rat adrenal gland. The perfusion of pinacidil (30-300 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), high $K^{+}$ (56 mM), DMPP (100 uM for 2 min), McN-A-343 (100 uM for 2 min), cyclopiazonic acid (10 uM for 4 min) and Bay-K-8644 (10 uM for 4 min). Also, under the presence of minoxidil (100 uM), which is also known to be a potassium channel activator, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with pinacidil (100 uM) under the presence of glibenclamide (1 uM), an antidiabetic sulfonylurea that has been shown to be a specific blocker of ATP-regulated potassium channels (for 20 min), CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were considerably recovered to a considerable extent of the normal release as compared to that of pinacidil only. These results, taken together, suggest that pinacidil cause the marked 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 suggest strongly that these potassium channel openers-sensitive membrane potassium channels also play an important role in regulating CA secretion.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.361-365
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• 2009

Effects of quercetin, a kind of flavonoids, on the vasodilating actions were investigated. Among the mechanisms for quercetin-induced vasodilatation in rat aorta, the involvement with the $Ca^{2+}$ activated $K^+$ ($K_{Ca}$) channel was examined. Pretreatment with NE ($5\;{\mu}M$) or KCl (60 mM) was carried out and then, the modulation by quercetin of the constriction was examined using rat aorta ring strips (3 mm) at $36.5^{\circ}C$. Quercetin (0.1 to $100\;{\mu}M$) relaxed the NE-induced vasoconstrictions in a concentrationdependent manner. NO synthesis (NOS) inhibitor, NG-monomethyl-L-arginine acetate (L-NMMA), at $100\;{\mu}M$ reduced the quercetin ($100\;{\mu}M$)-induced vasodilatation from $97.8{\pm}3.7%$ (n=10) to $78.0{\pm}11.6%$ (n=5, p<0.05). Another NOS inhibitor, L-NG-nitro arginine methyl ester (L-NAME), at $10\;{\mu}M$ also had the similar effect. In the presence of both $100\;{\mu}M$ L-NMMA and $10\;{\mu}M$ indomethacin, the quercetin-induced vasodilatation was further attenuated by $100\;{\mu}M$ tetraethylammonium (TEA, a $K_{Ca}$ channel inhibitor). Also TEA decreased the quercetin-induced vasodilatation in endothelium-denuded rat aorta. Used other $K_{Ca}$ channel inhibitors, the quercetin-induced vasodilatation was attenuated by $0.3\;{\mu}M$ apamin (a SK channel inhibitor), but not by 30 nM charybdotoxin (a BK and IK channel inhibitor). Quercetin caused a concentration-dependent vasodilatation, due to the endotheliumdependent and -independent actions. Also quercetin contributes to the vasodilatation selectively with SK channel on smooth muscle.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.3
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• pp.223-228
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• 2013

The calcium-activated $K^+$ ($BK_{Ca}$) channel is one of the potassium-selective ion channels that are present in the nervous and vascular systems. $Ca^{2+}$ is the main regulator of $BK_{Ca}$ channel activation. The $BK_{Ca}$ channel contains two high affinity $Ca^{2+}$ binding sites, namely, regulators of $K^+$ conductance, RCK1 and the $Ca^{2+}$ bowl. Lysophosphatidic acid (LPA, 1-radyl-2-hydroxy-sn-glycero-3-phosphate) is one of the neurolipids. LPA affects diverse cellular functions on many cell types through G protein-coupled LPA receptor subtypes. The activation of LPA receptors induces transient elevation of intracellular $Ca^{2+}$ levels through diverse G proteins such as $G{\alpha}_{q/11}$, $G{\alpha}_i$, $G{\alpha}_{12/13}$, and $G{\alpha}s$ and the related signal transduction pathway. In the present study, we examined LPA effects on $BK_{Ca}$ channel activity expressed in Xenopus oocytes, which are known to endogenously express the LPA receptor. Treatment with LPA induced a large outward current in a reversible and concentration-dependent manner. However, repeated treatment with LPA induced a rapid desensitization, and the LPA receptor antagonist Ki16425 blocked LPA action. LPA-mediated $BK_{Ca}$ channel activation was also attenuated by the PLC inhibitor U-73122, $IP_3$ inhibitor 2-APB, $Ca^{2+}$ chelator BAPTA, or PKC inhibitor calphostin. In addition, mutations in RCK1 and RCK2 also attenuated LPA-mediated $BK_{Ca}$ channel activation. The present study indicates that LPA-mediated activation of the $BK_{Ca}$ channel is achieved through the PLC, $IP_3$, $Ca^{2+}$, and PKC pathway and that LPA-mediated activation of the $BK_{Ca}$ channel could be one of the biological effects of LPA in the nervous and vascular systems.

• Proceedings of the PSK Conference
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• 2003.10a
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• pp.94-95
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• 2003

Local cytosolic rises of $Ca^{2+}$ appears to be critical in the regulation of many cellular activities, including muscle contraction, neurotransmitter secretion, and cell death. Cardiac $Ca^{2+}$ signaling similarly begins with discrete and localized rises of $Ca^{2+}$($Ca^{2+}$ sparks) triggered by $Ca^{2+}$ current ($I_{Ca}$). The large local releases of $Ca^{2+}$ in turn modulate L-type $Ca_{v}$1.2( ${\alpha}_{1C}$ $Ca^{2+}$ channels, suggesting that discrete $Ca^{2+}$ cross-signaling may occur in the micro-domains of ${\alpha}_{1C}$/ryanodine receptors (RyRs). (omitted)

• Molecules and Cells
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• v.21 no.1
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• pp.52-62
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• 2006

In previous reports we demonstrated that ginsenosides, active ingredients of Panax ginseng, affect some subsets of voltage-dependent $Ca^{2+}$ channels in neuronal cells expressed in Xenopus laevis oocytes. However, the major component(s) of ginseng that affect cloned $Ca^{2+}$ channel subtypes such as ${\alpha}_{1C}$(L)-, ${\alpha}_{1B}$(N)-, ${\alpha}_{1A}$(P/Q)-, ${\alpha}_{1E}$(R)- and ${\alpha}_{1G}$(T) have not been identified. Here, we used the two-microelectrode voltage clamp technique to characterize the effects of ginsenosides and ginsenoside metabolites on $Ba^{2+}$ currents ($I_{Ba}$) in Xenopus oocytes expressing five different $Ca^{2+}$ channel subtypes. Exposure to ginseng total saponins (GTS) induced voltage-dependent, dose-dependent and reversible inhibition of the five channel subtypes, with particularly strong inhibition of the ${\alpha}_{1G}$-type. Of the various ginsenosides, $Rb_1$, Rc, Re, Rf, $Rg_1$, $Rg_3$, and $Rh_2$, ginsenoside $Rg_3$ also inhibited all five channel subtypes and ginsenoside $Rh_2$ had most effect on the ${\alpha}_{1C}$- and ${\alpha}_{1E}$-type $Ca^{2+}$ channels. Compound K (CK), a protopanaxadiol ginsenoside metabolite, strongly inhibited only the ${\alpha}_{1G}$-type of $Ca^{2+}$ channel, whereas M4, a protopanaxatriol ginsenoside metabolite, had almost no effect on any of the channels. $Rg_3$, $Rh_2$, and CK shifted the steady-state activation curves but not the inactivation curves in the depolarizing direction in the ${\alpha}_{1B}$- and ${\alpha}_{1A}$-types. These results reveal that $Rg_3$, $Rh_2$ and CK are the major inhibitors of $Ca^{2+}$ channels in Panax ginseng, and that they show some $Ca^{2+}$ channel selectivity.

• Proceedings of the Korean Biophysical Society Conference
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• 1999.06a
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• pp.56-56
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• 1999

Change of membrane property can affect the activity of membrane proteins. In this work, we investigated the single channel properties of large conductance $Ca^{2+}$-activated $K^{+}$(BK) channels in planar lipid bilayers of different thickness. First, we recorded the activity of single BK channels from rat skeletal muscle incorporated into the control bilayer, then increased the bilayer thickness by perfusing the recording solution with the one saturated with n-pentane, or reduced the thickness by adding diheptanoylphosphatidylcholine (di$C_{7:0}$PC) to the recording soluton.(omitted)

• Proceedings of the Korean Biophysical Society Conference
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• 1996.07a
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• pp.34-34
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• 1996

Previously we showed that $Ba^{2+}$ block of large conductance $Ca^{2+}$-activated $K^{+}$ (BK) channel was larger in the planar lipid bilayer formed with negatively-charged phosphatidylserine (PS) than neutral phosphatidylethanolamine (PE). In this work, have studied the blocking effect of two $K^{+}$ channel blockers with different mechanisms of action, $Ba^{2+}$ and tetraethylammonium (TEA), on BK channels of rat skeletal muscle. (omitted)itted)

• Journal of the Institute of Electronics Engineers of Korea CI
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• v.46 no.4
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• pp.87-93
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• 2009

Wireless mesh networks (WMNs) are emerging technologies that provide ubiquitous environments and wireless broadband access. The aggregate capacity of WMNs can be improved by minimizing the effect of channel interference. The IEEE 802.11b/g standard which is mainly used for the network interface technology in WMNs provides 3 multiple channels. We must consider the channel scanning delay and the channel dependency problem to effectively assign channels in like these multi-channel WMNs. This paper proposes a cluster-based channel assignment (CB-CA) algorithm for multi-channel WMNs to solve such problems. The CB-CA does not perform the channel scanning and the channel switching through assigning co-channel to the inter-cluster head (CH) links. In the CB-CA, the communication between the CH and cluster member (CM) nodes uses a channel has no effect on channels being used by the inter-CH links. Therefore, the CB-CA can minimize the interference within multi-channel environments. Our simulation results show that CB-CA can improve the performance of WMNs.

• Proceedings of the Korean Biophysical Society Conference
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• 2002.06b
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• pp.35-35
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• 2002

The large conductance $Ca^{2＋}$ -activated $K^{＋}$ channels ($BK_{Ca}$) in vascular smooth muscle have been considered to function as a negative feedback in pressure-induced vasoconstriction. In the present study, the function of cytoskeletons in the regulation of $BK_{Ca}$ and its stretch sensitivity was investigated. Using the inside-out patch clamp technique, we recorded single channel activities of $BK_{Ca}$ with 150 mM KCl in the bath solution (pCa=6.5).(omitted)itted)

• Journal of Photoscience
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• v.4 no.1
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• pp.23-30
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• 1997

Leaf movements in nyctinastic plants are produced by changes in the turgor of extensor and flexor cells, collectively called motor cells, in opposing regions of the leaf movement organ, the pulvinus. In Samanea saman, a tropical tree of the legume family, extensor cells shrink and flexor cells swell to bend the pulvinus and fold the leaf at night, whereas extensor cells swell and flexor cells shrink to straighten the pulvinus and extend the leaf in the daytime. These changes are caused by ion fluxes primarily of potassium and chloride, across the plasma membrane of the motor cells. These ion fluxes are regulated by exogenous light signals and an endogenous biolgical clock. Inward-directed K$^+$ channels are closed in extensor and open in flexor cells in the dark period, while these channels are open in extensor and closed in flexor cells in the light period. Blue light opens the closed K$^+$ channels in extensor and closes the open them in flexor cells during darkness. Illumination of red light followed by darkness induces to open the closed K$^+$ channels in flexor and to close the open K$^+$ channels in extensor cells in the light. The dynamics of K$^+$ channels in motor cells that are controlled by light signals are consistent with the behavior of the pulvini in intact plants. Therefore, these cell types are an attractive model system to elucidate regulations of ion transports and their signal transduction pathways in plants. This review is focused on light-controlled ion movements and regulatory mechanisms involved in phosphoinositide signaling in leaf movements in nyctinastic plants.