• Biomolecules & Therapeutics
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• 제15권4호
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• pp.212-217
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• 2007

In atrial myocytes, lacking t-tubules, $Ca^{2+}$ current ($I_{Ca}$)-initiated $Ca^{2+}$ release at the peripheral junctional sites propagates into the interior of the cell by diffusion of $Ca^{2+}$. We have previously reported that time of activation of the central sites is independent of $I_{Ca}$. In the present study we have probed the effects of Bay K 8644 on $Ca^{2+}$ propagation wave to the center of the myocyte using rapid 2-D confocal $Ca^{2+}$ imaging in the rat atrial myocytes. Enhancement of $I_{Ca}$ by Bay K 8644 accelerated the rate of peripheral $Ca^{2+}$ release, but did not affect the speed of propagation of central release. In contrast, enhancement of $I_{Ca}$ by intracellular cAMP reduced the magnitude of peripheral and central $Ca^{2+}$ transients, but significantly accelerated the speed of central $Ca^{2+}$ release. Our data suggest that the speed of central $Ca^{2+}$ propagation triggered by $I_{Ca}$ is not regulated by the magnitude of either $I_{Ca}$ or local cytosolic $Ca^{2+}$ releases.

• The Korean Journal of Physiology
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• 제30권1호
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• pp.1-9
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• 1996

The objective of the present study was to characterize the role of adenosine in regulation of ATP-sensitive $K^+\;channel\;(K_{ATP}\;channel)$ activity in isolated rabbit ventricular myocytes using the patch clamp technique. Internal adenosine had little effects on KaTr channel activity. In an outside-out patch with intrapipette GTP and ATP, external adenosine stimulated $K_{ATP}\;channel$ activity. In an inside-out Patch with intrapipette adenosine, ATP reduced $K_{ATP}\;channel$ activity, and GTP stimulated $K_{ATP}\;channel$ activity. Adenosine receptor activation shifted the half-maximal inhibition Of $K_{ATP}\;channel\;from\;70\;to\;241\;{\mu}m$. These results Suggest that activation of adenosine receptors stimulates $K_{ATP}\;channels$ in rabbit ventricular myocytes by reducing the apparent affinity of the channel for ATP. The effect may be important for activating $K_{ATP}\;channels$ during early phase of myocardial ischemia.

• The Korean Journal of Physiology
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• 제26권2호
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• pp.99-111
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• 1992

Permissive action of thyroid hormone at the level of Ca channel and responsible mechanisms underlying thyroid hormone-induced change in myocardial contractile state and $T_3-induced$ arrhythmias were investigated in rabbit ventricular or atrial myocytes using whole cell patch clamp technique. Single cells were isolated by Langendorff perfusion with collagenase. Cardiac myocytes were incubated in $low-Cl^-,$, $high-K^+$ medium containing $1_{\mu}M\;L-triiodothyronine\;(T_3)$ at $4^{\circ}C$ for 2.10 hours. The calcium currrent $(I_{Ca})$ was increased in $T_3$ loaded cells, however, the shape of current voltage curve and reverse potential did not altered. Cyclic AMP, cyclic GMP, isoprenaline and 3-isobutyl-1-methyl-xanthine increased $I_{Ca}$ in euthyroid and hyperthyroid conditions, and acetylcholine blocked the increase of $I_{Ca}\;in\;T_3$ loaded cells. The amplitude of $I_{Ca}$ was much larger after perfusing cGMP than cGMP in both conditions, whereas the degree of increase of $I_{Ca}$ was greater after perfusing cAMP than cGMP in $T_3$ loaded cells. The degree of increase of $I_{Ca}$ after perfusing isoprenaline or IBMX also was greater in $T_3$ loaded cells than in control cells. Background current induced by isoprenaline also increased in $T_3$ loaded cells. The Ca release dependent inward current was increased in amplitude but its activation and inactivation time course was not changed in $T_3$ loaded cells. Activation of Na pump current was not changed in $T_3$ loaded cells. From the above results it is suggested that thyroid hormone induced increase in the contractile state of cardiac myocytes are accompanied by augmented $I_{Ca}$ and the increase of Ca release from sarcoplasmic reticulum and the permissive action of thyroid hormone to catecholamines could induce arrhythmias through the increase of $I_{Ca}$ and background current.

• 대한수의학회지
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• 제38권1호
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• pp.29-42
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• 1998

$Mg^{2+}$ is one of the most abundant divalent cations in mammalian body(0.2~1.0mM) and the important physiological roles are : first, the cofactor of many enzyme activities, second, the regulator of glycolysis and DNA synthesis, third, the important role of bioenergetics by regulating of phosphorylation, fourth, the influence of cardiac metabolism and function. In this work we have investigated the regulation of the $Mg^{2+}$ induced by ${\alpha}_1-adrenoceptor$ stimulation in perfused guinea pig hearts and isolated myocytes. The $Mg^{2+}$ content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. The elimination of $Mg^{2+}$ in the medium increased the force of contraction of right ventricular papillary muscles, and the left ventricular pressure. Phenylephrine also enhanced the force of contraction in the presence of $Mg^{2+}-free$ medium. ${\alpha}_1-Agonists$ such as phenylephrine and methoxamine were found to induce $Mg^{2+}$ efflux in both perfused hearts and myocytes. These effects were blocked by prazosin, an ${\alpha}_1-adrenoceptor$ antagonist. The $Mg^{2+}$ influx could also be induced by phenylephrine and R59022, a diacylglycerol kinase inhibitor. In the presence of protein kinase C(PKC) inhibitors, phenylephrine produced an increase in $Mg^{2+}$ efflux from perfused hearts. Furthermore, $Mg^{2+}$ efflux by phenylephrine was amplified by phorbol 12-myristate 13-acetate(PMA). This enhancement of $Mg^{2+}$ efflux by PMA was blocked by prazosin in perfused hearts. By contrast, the $Mg^{2+}$ influx could be induced by verapamil, nifedipine, ryanodine in perfused hearts, but not in myocytes. $W^7$, a $Ca^{2+}$/calmodulin antagonist, completely blocked the phenylephrine-induced $Mg^{2+}$ efflux in perfused hearts. In conclusion, $Mg^{2+}$ is responsible for the cardiac activity associated with ${\alpha}_1-adrenoceptor$ stimulation. The mobilization of $Mg^{2+}$ is decreased or increased by ${\alpha}_1-adrenoceptor$ stimulation in guinea pig hearts. These responses may be related specifically to the respective pathways of signal transduction. A decrease in $Mg^{2+}$ efflux by ${\alpha}_1-adrenoceptor$ stimulation in hearts can be through PKC dependent and intracellular $Ca^{2+}$ levels.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1998년도 학술발표회
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• pp.37-37
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• 1998

Effects of endothelin-l (ET-l) on contraction, $Ca^{2＋}$ transient and L -type $Ca^{2＋}$ current ( $I_{Ca,L}$) were investigated in single ventricular myocytes isolated from guinea-pig hearts. ET-l at concentrations of 5 and 10 nM produced a biphasic pattern of inotropism： a first decrease in contraction by 34.4$\pm$2.5 ％ of the control followed by a sustained increase in contraction by 66.6$\pm$8.4% (mean$\pm$S.E.M., n=9).(omitted)

• 제어로봇시스템학회:학술대회논문집
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• 제어로봇시스템학회 2005년도 ICCAS
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• pp.1179-1182
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• 2005

To facilitate the cell based robot research, we presented a micro-mechanical force measurement system for the biological muscle actuators, which utilize glucose as a power source for potential application in a human body or blood vessels. The system is composed of a micro-manipulator, a force transducer with a glass probe, a signal processor, an inverted microscope and video recoding system. Using this measurement system, the contractile force and frequency of the cardiac myocytes were measured in real time and the magnitude of the contractile force of each cardiac myocyte on a different condition was compared. From the quantitative experimental results, we estimated that the force of cardiac myocytes is about $20{\sim}40\;{\mu}$N, and showed that there is difference between the control cells and the micro-patterned cells.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.58-58
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• 2001

Even though atrial fibrillation is the most prevalent arrhythmia, the mechanism of development is not yet clear. Recently, there has been several reports that the most frequent source of paroxysmal atrial fibrillation is located inside pulmonary vein. Recently we successfully isolated single cardiac myocytes which were inside of pulmonary vein and reported the spontaneous action potential was generated from these cells.(omitted)

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.54-54
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• 2001

The effects of protein kinase C inhibitors, chelerythrine and bisindolylmaleimide I, on acetylcholine activated $K^{＋}$ currents ( $I_{KACh}$) were examined in atrial myocytes of mice using patch clamp technique. Chelerythrine and bisindolylmaleimide I inhibited $I_{KACh}$ in reversible and dose-dependent manners. Half maximal effective concentrations were 0.49 $\pm$ 0.01 $\mu$M for chelerythrine and 98.69 $\pm$ 12.68 nM for bisindolylmaleimide I.(omitted)

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 공동 춘계학술대회
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• pp.81.1-81
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• 2000

No Abstract, See Full Text

• The Korean Journal of Physiology
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• 제27권2호
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• pp.151-162
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• 1993

In order to investigate the effect of intracellular cyclic GMP on calcium current the whole-cell patch clamp technique with internal perfusion method was used in isolated ventricular myocytes of the rabbit. Cyclic GMP, 8-bromo-cyclic GMP, cyclic AMP, isoprenaline and forskolin were perfused into cells and their effects on calcium current were analysed by applying depolarizing step pulses of + 10 mV in amplitude far 300 msec from holding potential of - 40 mV. Not only cyclic AMP $(100\;{\mu}M)$ but also cyclic GMF $(100\;{\mu}M)$ increased the basal calcium current. 8-Bromo-cyclic GMP $(100\;{\mu}M)$, a good stimulator of the cyclic GMP-dependent protein kinase, also increased the basal calcium current and its peak amplitude of calcium current was larger than that in the presence of cyclic AMP or cyclic GMP alone. In the presence of $100\;{\mu}M$ cyclic GMP or $100\;{\mu}M$ 8-bromo-cyclic GMP, already augmented calcium current was potentiated by intracellular application of $100\;{\mu}M$ cyclic AMP or $1\;{\mu}M$ isoprenaline or $1\;{\mu}M$ forskolin. In the presence of cyclic GMP, acetylcholine reduced the calcium current only when the calcium current was increased by isoprenaline. From the above results it could be concluded that intracellular perfusion with cyclic GMP increases the basal calcium current via a mechanism involving a cyclic GMP-dependent protein kinase.