• The Korean Journal of Physiology and Pharmacology
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• 제24권6호
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• pp.529-543
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• 2020

In contrast to ventricular myocytes, the structural and functional importance of atrial transverse tubules (T-tubules) is not fully understood. Therefore, we investigated the ultrastructure of T-tubules of living rat atrial myocytes in comparison with ventricular myocytes. Nanoscale cell surface imaging by scanning ion conductance microscopy (SICM) was accompanied by confocal imaging of intracellular T-tubule network, and the effect of removal of T-tubules on atrial excitation-contraction coupling (EC-coupling) was observed. By SICM imaging, we classified atrial cell surface into 4 subtypes. About 38% of atrial myocytes had smooth cell surface with no clear T-tubule openings and intracellular T-tubules (smooth-type). In 33% of cells, we found a novel membrane nanostructure running in the direction of cell length and named it 'longitudinal fissures' (LFs-type). Interestingly, T-tubule openings were often found inside the LFs. About 17% of atrial cells resembled ventricular myocytes, but they had smaller T-tubule openings and a lower Z-groove ratio than the ventricle (ventricular-type). The remaining 12% of cells showed a mixed structure of each subtype (mixed-type). The LFs-, ventricular-, and mixed-type had an appreciable amount of reticular form of intracellular T-tubules. Formamide-induced detubulation effectively removed atrial T-tubules, which was confirmed by both confocal images and decreased cell capacitance. However, the LFs remained intact after detubulation. Detubulation reduced action potential duration and L-type Ca²⁺ channel (LTCC) density, and prolonged relaxation time of the myocytes. Taken together, we observed heterogeneity of rat atrial T-tubules and membranous ultrastructure, and the alteration of atrial EC-coupling by disruption of T-tubules.

• Biomolecules & Therapeutics
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• 제14권1호
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• pp.19-24
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• 2006

Atrial chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances, which initiates arrhythmia. Atrial myocytes, lacking t-tubules, have two functionally separate sarcoplasmic reticulums (SRs): those at the periphery close to the surface membrane, and those at the cell interior (center) not associated with the membrane. To explore possible role of fluid pressure (FP) in the regulation of atrial local $Ca^{2+}$ signaling we investigated the effect of FP on subcellular $Ca^{2+}$ signals in isolated rat atrial myocytes using confocal microscopy. FP was applied to whole area of single myocyte with pressurized automatic micro-jet (200-400 $mmH_2O$) positioned close to the cell. Application of FP enhanced spontaneous occurrences of peripheral and central $Ca^{2+}$ sparks with larger effects on the peripheral release sites. Unitary properties of single sparks were not altered by FP. Exposure to higher FP often triggered longitudinal $Ca^{2+}$ wave. These results suggest that fluid pressure may directly alter excitability of atrial myocytes by activating $Ca^{2+}$-dependent ionic conductance in the peripheral membrane and by enhancing spontaneous activation of central myofilaments.

• Molecules and Cells
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• 제43권5호
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• pp.438-447
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• 2020

The aim of this study was to explore the role of IL-6-miR-210 in the regulation of Tregs function and atrial fibrosis in atrial fibrillation (AF). The levels of interleukin (IL)-6 and IL-10 in AF patients were detected by using ELISA. Proportions of Treg cells were detected by fluorescence activated cell sorting analysis in AF patients. The expression of Foxp3, α-SMA, collagen I and collagen III were determined by western blot. The atrial mechanocytes were authenticated by vimentin immunostaining. The expression of miR-210 was performed by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was used to predict potential targets of miR-210. The cardiomyocyte transverse sections in AF model group were observed by H&E staining. The myocardial filaments were observed by masson staining. The level of IL-6 was highly increased while the level of IL-10 (Tregs) was significantly decreased in AF patients as compared to normal control subjects, and IL-6 suppressed Tregs function and promoted the expression of α-SMA, collagen I and collagen III. Furthermore, miR-210 regulated Tregs function by targeting Foxp3, and IL-6 promoted expression of miR-210 via regulating hypoxia inducible factor-1α (HIF-1α). IL-6-miR-210 suppresses regulatory T cell function and promotes atrial fibrosis by targeting Foxp3.

• The Korean Journal of Physiology
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• 제22권2호
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• pp.219-230
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• 1988

The effect of glycine, structurally the most simple amino acid was investigated on the electrophysiological characteristics of the isolated superfused atrial muscle and sinus node cells of the rabbit heart. Superfusion of the sinus node cell with glycine solution (3, 5 and 8 mM) produced concentration-dependent increments of OS (overshoot potential) and MDP (maximum diastolic potential). Generally action potential amplitude increased as a result of greater increment of OS than that of MDP. The changes in action potential of the sinus node cell peaked in $7{\sim}10{\;}minutes$ after onset of superfusioin. On the contrary to the response to intravenously administered glycine, the rate of spontaneous firing of sinus node cell was invariably increased following superfusion with glycine. Action potential duration manifested as $APD_{60}$ (time to 60% repolarization) was significantly shortened by glycine. And the electrophysiological effects of glycine on the atrial muscle cell were similar to that on the sinus node cells. The results of present study suggest that glycine can exert direct effects on the atrial muscle and sinus node cells of the rabbit heart.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1998년도 학술발표회
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• pp.38-38
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• 1998

Resting membrane potential of atrial myocytes is less negative than K+ equilibrium potential, suggesting the presence of ion channels carrying inward currents. We investigated the background Na$\^$＋/ current in rat atrial myocytes using both conventional whole cell voltage clamp technique and single channel recording.(omitted)

• 대한기계학회:학술대회논문집
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• 대한기계학회 2008년도 추계학술대회A
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• pp.1669-1673
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• 2008

In this study, we simulated the atrial arrhythmia numerically. By using electro-physiological model of atrial cell from Nygren et al. and applying reaction-diffusion partial differential equation, we simulated electrical conduction in atrium. A 3-D mesh system representing the human atrium was reconstructed from the surface geometry of atrium. We used a stimulus in the form of an archetype around pulmonary vessels in the left atrium to cause the atrial arrhythmia. The septal atrial tarchycardia was developed after the stimulus.

• 약학회지
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• 제48권6호
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• pp.352-357
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• 2004

Atrial myocytes have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery colocalized with L-type $Ca^{2+}$channels (DHPRS) and those a t the cell interior not associated with DHPRs. $Ca^{2+}$ current ($I_{ca}$) directly gates peripheral RyRs on action potential and the subsequent peripheral $Ca^{2+}$ release propagates into the center of atrial myocytes. The mechanisms that regulate the $Ca^{2+}$+ propagation wave remain Poorly understood. Using 2-D confocal$Ca^{2+}$ imaging, we examined the role of inositol 1,4,5-trisphosphate receptor (IP $_3R$) and mitochondria on ($I_{ca}$)- gated local $Ca^{2+}$ signaling in rat atrial myocytes. Blockade of IP $_3R$ by xestospongin C (XeC) partially suppressed the magnitudes of I ca-gated central and peripheral $Ca^{2+}$ releases with no effect on $I_{ca}$. Mitochondrial staining revealed that mitochondria were aligned with ${\thickapprox}2-{\mu}m$ separations in the entire cytoplasm of ventricular and atrial myocytes. Membrane depolarization induced rapid mitochondrial $Ca^{2+}$ rise and decay in the cell periphery with slower rise in the center, suggesting that mitochondria may immediately uptake cytosolic $Ca^{2+}$, released from the peripheral SR on depolarization, and re-release the $Ca^{2+}$ into the cytosol to activate neighboring central RyRs. Our data suggest that the activation of IP $_3R$ and mitochondrial $Ca^{2+}$ handing on action potential may serve as a cofactor for the $Ca^{2+}$ propagation from the DHPR-coupled RyRs to the DHPR-uncoupled RyRs with large gaps between them.

• The Korean Journal of Physiology
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• 제26권1호
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• pp.27-35
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• 1992

We used the whole cell patch clamp technique to examine the ionic basis for the tail current after depolarizing pulse in single atrial myocytes of the rabbit. We recorded the tail currents during various repolarizations after short depolarizing pulse from a holding potential of -70 mV. The potassium currents were blocked by external 4-aminopyridine and replacement of internal potassium with cesium. The current was reversed to the outward direction above +10 mV. High concentrations of intracellular calcium buffer inhibited the activation of the current. Diltiazem and ryanodine blocked it too. These data suggest that the current is activated by intracellular calcium released from sarcoplasmic reticulumn. When the internal chloride concentration was increased, the inward tail current was increased. The current was partially blocked by the anion transport blocker niflumic acid. The current voltage curve of the niflumic acid sensitive current component shows outward rectification and is well fitted to the current voltage curve of the theoretically predicted chloride current calculated from the constant field equation. The currents recorded in rabbit atrial myocytes, with the method showing isolated outward Na Ca exchange current in ventricular cells of the guinea pig, suggested that chloride conductance could be activated with the activation of Na/ca exchange current. From the above results it is concluded that a chloride sensitive component which is activated by intracellular calcium contributes to tail currents in rabbit atrial cells.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.31-31
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• 2003

Cardiac atrium is now well-known as an endocrine organ which secretes atrial natriuretic peptide (AMP), participating in the regulation of body fluid and blood pressure. ANP is released mainly from cardiac muscle cells in response to various physiological and pathological conditions to induce atrial stretch. Ca$\^$2+/ may be one of the most important factors affecting ANP secretion even though controversy still persists. The aim of the present study is to investigate the effect of lysophosphatidylcholines (LPCs) and moxonidine on atrial hemodynamics and ANP secretion in hypertrophied atria. LPC is an endogenous phospholipid released from cell membrane during ischemia, and moxonidine is a imidazoline 1 (Il) receptor agonoist.

• The Korean Journal of Physiology
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• 제23권2호
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• pp.339-350
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• 1989

Electrophysiological effects of ammonia was studied in the isolated superfused sinus node and atrial muscle cells of the rabbit heart. No significant changes were observed in the overshoot potential (05), maximum diastolic potential (MDP), and action potential amplitude (APA) of the sinus node cells following superfusion with 3.0 mM ammonia, fifty times upper limit of the normal human plasma level. However the action potential duration (APD) of sinus node cells were significantly prolonged after superfusion with 0.6 mM ammonia for 20 min or with 1.2 and 3.0 mM ammonia for 5 minutes. Ammonia in all the concentrations tested decreased the rate of spontaneous firing (RSF) from the sinus node cells. After superfusion of sinus node cells with 0.3 mM ammonia for 20 min, the RSF significantly decreased from 20 min to 25 min after onset of superfusion while a significant decrement in the RSF was observed from 7 min to 30 min following superfusion with 3.0 mM ammonia for S min. On the other hand, the effects of ammonia on the action potential of the rabbit atrial muscle cell were much similar to those on pacemaker cells except that the atrial cell was generally less sensitive to ammonia. The results suggest that ammonia may cause changes in the action potential of the rabbit cardiac cells by the direct action, and that the cardiac effects of ammonia are generally opposite to those of glycine.