• Proceedings of the Ginseng society Conference
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• 2005.11a
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• pp.32-40
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as Ca$^{2+}$, K$^+$, Na$^+$, Cl$^-$, or ligand gated ion channels (i.e. 5-HT$_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent Ca$^{2+}$, K$^+$, and Na$^+$ channels, whereas ginsenosides activate Ca$^{2+}$-activated Cl$^-$ and Ca$^{2+}$-activated K$^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as 5-HT$_3$. nicotinic acetylcholine, and NMDA receptors. This presentation will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities as a ligand as other drugs do.

• Journal of Animal Science and Technology
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• v.66 no.3
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• pp.443-456
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• 2024

In female tract, mammalian sperm develop hyperactivated motility which is a key physiological event for sperm to fertilize eggs. This motility change is triggered by Ca²⁺ influx via the sperm-specific Ca²⁺ channel, CatSper. Although previous studies in human and mice largely contributed to understanding CatSper and Ca²⁺ signaling for sperm hyperactivation, the differences on their activation mechanisms are not well understood yet. There are several studies to examine expression and significance of the CatSper channel in non-human and non-mouse models, such as domestic animals. In this review, I summarize key knowledge for the CatSper channel from previous studies and propose future aspects for CatSper study using sperm from domestic animals.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.5
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• pp.413-421
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• 2001

An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of $K^+$ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured $Ca^{2+}-activated\;K\;(K_{Ca})$ currents and delayed rectifier K $(K_{dr})$ currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of $K_{Ca}$ channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of $K_{Ca}$ channel to $Ca^{2+}$ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of $K_{Ca}$ channel by TEA were more sensitive in hypertrophy. $K_{dr}$ current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of $K_{dr}$ current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of $K_{Ca}$ channels and $K_{dr}$ channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.225-232
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• 1995

The present study was conducted to evaluate the effect of phorbol 12,13-dibutyrate (PDBu) on the contraction of rabbit jugular vein in vitro. PDBu concentrations of greater than 10 nM induced a periodic contraction which was composed of rapid contraction, plateau and slow relaxation. The frequency of periodic contraction increased as PDBu concentration increased. The PDBu-induced contraction was inhibited by staurosporine (100 nM), it was not changed by tetrodotoxin $(1\;{\mu}M).$ In $Ca^{2+}$-free medium, PDBu induced a sustaining contraction, but not periodic contraction. Addition of $Ca^{2+}$ to medium evoked periodic contraction which was inhibited by nifedipine, PDBu concentrations of greater than $0.1\;{\mu}M$ increased ^{45}Ca^{2+}$ uptake without changing $^{45}Ca^{2+}$ efflux. Charybdotoxin and apamin, $Ca^{2+}$-activated K^{+}$ channel blockers, did not affect the PDBu-induced periodic contraction, whereas tetraethylammonium (TEA) abolished the periodicity. Pinacidil $(10\;{\mu}M).$, a potassium channel activator, blocked PDBu induced periodic contraction, which was recovered by glybenclamide $(10\;{\mu}M).$. In high potassium solution, PDBu did not produce the periodic contraction. These results suggest that the PDBu-induced periodicity of contraction is modulated by voltage dependent $Ca^{2+}$ channel and ATP-sensitive $K^{+}$ channel.

• Development and Reproduction
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• v.7 no.2
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• pp.81-88
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• 2003

Initiation and activation of sperm motility are prerequisite processes for the contact and fusion of male and female gametes at fertilization. The phenomena are under the regulation of CAMP and $Ca^{2+}$ in vertebrates and invertebrates. Mammalian sperm requires $Ca^{2+}$and cyclic AMP for the activation of sperm motility. Cell signaling for the initiation and activation of sperm motility has been well studied in the ascidians, Ciona intestinalis and C. savignyi and salmonid fishes. In Ciona, whose cell signaling for activation of sperm motility has been established, the sperm-activating and -attracting factor released from unfertilized egg requires extracellular $Ca^{2+}$ for activating sperm motility and eliciting chemotactic behavior of the activated sperm toward the egg. On the other hand, the cyclic AMP-dependent phosphorylation of protein is essential for the initiation of sperm motility in salmonid fishes. A decrease in the environmental Ti concentration surrounding the spawned sperm causes a li efflux and $Ca^{2+}$ influx through the specific $K^{+}$ channel and dihydropyridine-sensitive L-/T- type $Ca^{2+}$ channel, respectively, thereby leading to the membrane hyperpolarization and $Ca^{2+}$ influx. The membrane hyperpolarization synthesizes cyclic AMP, which triggers the luther Process of cell signaling, i.e., cyclic AMP-dependent protein phosphorylation, to initiate sperm motility in salmond fishes.almond fishes.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.547-554
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• 1999

The aim of the present study is to investigate the contribution of $Ca^{2+} ?activated\;K^+\;(K_{Ca})$ channels and delayed rectifier $K^+\;(K_V)$ channels to the resting membrane potential (RMP) in rabbit middle cerebral arterial smooth muscle cells. The RMP and membrane currents were recorded using the whole-cell patch configuration and single $K_{Ca}$ channel was recorded using the outside-out patch configuration. Using the pipette solution containing 0.05 mM EGTA, the RMP was $-25.76{\pm}5.08$ mV (n=12) and showed spontaneous transient hyperpolarizations (STHPs). The membrane currents showed time- and voltage-dependent outward currents with spontaneous transient outward currents (STOCs). When we recorded the membrane potential using the pipette solution containing 10 mM EGTA, the RMP was depolarized and did not show STHPs. The membrane currents showed no STOCs but only showed slowly inactivating outward currents. External TEA (1 mM) reversibly inhibited the STHPs, depolarized the RMP, reduced the membrane currents, abolished STOCs, and decreased the open probability of single $K_{Ca}$ channel. When $K_V$ currents were isolated, the application of 4-AP (5 mM) depolarized the RMP. The important aspect of our results is that $K_{Ca}$ channel is responsible for the generation of the STHPs in the membrane potential and plays an important role in the regulation of the RMP and $K_V$ channel is also responsible for the regulation of the RMP in rabbit middle cerebral arterial smooth muscle cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.3
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• pp.743-748
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• 2005

This study was performed for the investigation of vasodilatory efficacy and its underlying mechanisms of Jagumhuan(JGH), a herbal remedy. JGH produced completely endothelium-dependent relaxation and relaxed phenylephrine(PE)-precontracted aorta in a concentration dependent manner. The magnitude of relaxation was greater in PE induced contraction than that of KCl, suggesting involvement of $K^+$ channel in the relaxant effect. Both glibenclamide$(10^{-5}M)$, a $K_{ATP}$ channel inhibitor and indometacin, a cyclooxygenase inhibitor, completely prevented this relaxation. The relaxation effects of JGH, involve in part the release of nitric oxide from the endothelium as pretreatment with L-NAME, an NOS inhibitor, and methylene blue, a cGMP inhibitor, attenuated the responses by 62% and 58%, respectively. In addition, nitrite was produced by JGH in human aortic smooth muscle cells and human umbilical vein endothelial cells. The relaxant effect of JGH was also inhibited by 55.41% by tetraethylammonium(TEA; 5mM), a $K_{Ca}$ channel inhibitor. In the absence of extracellular $Ca^{2+}$, pre-incubation of the aortic rings with JGH significantly reduced the contraction by PE, suggesting that the relaxant action of the JGH includes inhibition of $Ca^{2+}$ release from intracellular stores. These results indicate that in rat thoracic aorta, JGH may induce vasodilation through ATP sensitive $K^+$ channel activation by prostacyclin production. However, the relaxant effect of JGH may also mediated in part by NO pathways and $Ca^{2+}$ activated $K^+$ channel.

• Proceedings of the Korean Biophysical Society Conference
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• 1997.07a
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• pp.17-17
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• 1997

We investigated the relationship between the voltage-operated calcium channel current and the corresponding [Ca$^{2＋}$]i change (Ca$^{2＋}$-transient) in guinea-pig gastric myocyte. Fluorescence microspectroscopy was combined with conventional whole-cell patch clamp technique and fura-2 (80 $\mu$M) was added into the CsCl-rich pipette solution.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.2
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• pp.113-120
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• 2000

To investigate the mechanism of smooth muscle contraction induced by emptying of intracellular $Ca^{2+}$ stores, we measured isometric contraction and $^{45}Ca^{2+}$ influx. $CaCl_2$ increased $Ca^{2+}$ store emptying- induced contraction in dose-dependent manner, but phospholipase C activity was not affected by the $Ca^{2+}$ store emptying-induced contraction. The contraction was inhibited by voltage-dependent $Ca^{2+}$ channel antagonists dose dependently, but not by TMB-8 (intracellular $Ca^{2+}$ release blocker). Both PKC inhibitors (H-7 and staurosporine) and tyrosine kinase inhibitors (genistein and methyl 2,5-dihydroxycinnamic acid) significantly inhibited the contraction, but calmodulin antagonists (W-7 and trifluoperazine) had no inhibitory effect on the contraction. The combined inhibitory effects of protein kinase inhibitors, H-7 and genistein, together with verapamil were greater than that of each one alone. In $Ca^{2+}$ store-emptied condition, $^{45}Ca^{2+}$ influx was significantly inhibited by verapamil, H-7 or genistein but not by trifluoperazine. However combined inhibitory effects of protein kinase inhibitors, H-7 and genistein, together with verapamil were not observed. Therefore, this kinase pathway may modulate the sensitivity of contractile protein. These results suggest that contraction induced by emptying of intracellular $Ca^{2+}$ stores was mediated by influx of extracellular $Ca^{2+}$ through voltage-dependent $Ca^{2+}$ channel, also protein kinase C and/or tyrosine kinase pathway modulates the $Ca^{2+}$ sensitivity of contractile protein.

• Journal of Plant Biology
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• v.36 no.3
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• pp.233-239
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• 1993

Effect of Ca2+ on the conversion of 1-aminocycloprophane-1-carboxylic acid (ACC) to ethylene was studied with 2.5 day-old mung bean hypocotyl segments. The conversion of ACC in these tissues was inhibited by plasmolysis and sulfosuccinimidyl (hydroxyphenyl) propionate (sulfo-SHPP). The ACC induced ethylene production in HC (high calcium)-tissue grown on the Ca2+ added medium was greater than that in N (normal)-tissue. HC-tissue had a lower inhibition rate of ACC conversion by EGTA and Ca2+ -channel blockers than N-tissue. The rates of the ACC conversion by both kinds of tissues were stimulated by the Ca2+ ionophore A23187. From these results, we suggests a mechanism for the stimulative effect of Ca2+ on the conversion of ACC to ethylene as follows; in some tissues where ACC conversion is linked with plasma membrane, Ca2+ may be transported from apoplast through Ca2+ -channel into the cytoplasm ad stimulate ACC-oxidase activity.