Home About us Contact
|
Home About us Contact | ||
|
|
||
Atrial Cells (atrial + cell)
Selected AbstractsA Novel Background Potassium Channel in Rat Atrial CellsEXPERIMENTAL PHYSIOLOGY, Issue 4 2000Z. Shui A K+ channel activated by intracellular ATP has been observed in inside-out patches from rat atrial cells. The channel has a slope conductance of 130 ± 5 pS in symmetrical 140 mM K+ solution, and is almost independent of voltage over the range from -80 to +80 mV. There is no detectable inactivation during application of ATP over a few minutes. In the presence of 3 mM intracellular ATP, channel openings occur as bursts with a mean open time of 1.7 ms, a mean closed time of 0.4 ms, a mean burst duration of 18 ms and a mean burst interval of 41 ms. Kinetic analysis suggests that ATP mainly affects the burst duration and the burst interval of the channel. Based on the properties above, the channel differs from other known K+ channels in cardiac cells and may contribute to background K+ current. [source] Characterization of Sustained Atrial Tachycardia in Dogs with Rapid Ventricular Pacing-Induced Heart FailureJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2003Bruce S. Stambler M.D. Introduction: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. Methods and Results: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After20 ± 7 daysof rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length120 ± 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (,130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. Conclusions: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.(J Cardiovasc Electrophysiol, Vol. 14, pp. 499-507, May 2003) [source] Comparison of effects of acetylcholine on electromechanical characteristics in guinea-pig atrium and ventricleEXPERIMENTAL PHYSIOLOGY, Issue 1 2005W. J. Zang The direct negative effects of acetylcholine (ACh) on guinea-pig atria and ventricles were investigated using standard microelectrodes, a force transducer and a video edge-detection system. It was found that: (1) ACh (at 0.001,100 ,m) decreased the force of contraction and shortened the action potential duration (APD) in both atria and ventricles in a concentration-dependent manner, and that the atria were more sensitive to ACh than the ventricles; and (2) the direct negative inotropic effect of ACh (1 ,m) on an isolated cardiac cell was similar to that on the isolated myocardium. But this effect was not present in all isolated ventricular cells, while all the atrial cells responded to ACh. In conclusion, ACh had direct inhibitory effects on both atrial and ventricular tissue and myocytes, although the effects were greater in atria than in ventricles; and the negative inotropic effect of ACh was closely related to the shortening of the APD. [source] A Novel Background Potassium Channel in Rat Atrial CellsEXPERIMENTAL PHYSIOLOGY, Issue 4 2000Z. Shui A K+ channel activated by intracellular ATP has been observed in inside-out patches from rat atrial cells. The channel has a slope conductance of 130 ± 5 pS in symmetrical 140 mM K+ solution, and is almost independent of voltage over the range from -80 to +80 mV. There is no detectable inactivation during application of ATP over a few minutes. In the presence of 3 mM intracellular ATP, channel openings occur as bursts with a mean open time of 1.7 ms, a mean closed time of 0.4 ms, a mean burst duration of 18 ms and a mean burst interval of 41 ms. Kinetic analysis suggests that ATP mainly affects the burst duration and the burst interval of the channel. Based on the properties above, the channel differs from other known K+ channels in cardiac cells and may contribute to background K+ current. [source] One-Dimensional Rabbit Sinoatrial Node Models:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003Benefits, Limitations Introduction: Cardiac multicellular modeling has traditionally focused on ventricular electromechanics. More recently, models of the atria have started to emerge, and there is much interest in addressing sinoatrial node structure and function. Methods and Results: We implemented a variety of one-dimensional sinoatrial models consisting of descriptions of central, transitional, and peripheral sinoatrial node cells, as well as rabbit or human atrial cells. These one-dimensional models were implemented using CMISS on an SGI® Origin® 2000 supercomputer. Intercellular coupling parameters recorded in experimental studies on sinoatrial node and atrial cell-pairs under-represent the electrotonic interactions that any cardiomyocyte would have in a multidimensional setting. Unsurprisingly, cell-to-cell coupling had to be scaled-up (by a factor of 5) in order to obtain a stable leading pacemaker site in the sinoatrial node center. Further critical parameters include the gradual increase in intercellular coupling from sinoatrial node center to periphery, and the presence of electrotonic interaction with atrial cells. Interestingly, the electrotonic effect of the atrium on sinoatrial node periphery is best described as opposing depolarization, rather than necessarily hyperpolarizing, as often assumed. Conclusion: Multicellular one-dimensional models of sinoatrial node and atrium can provide useful insight into the origin and spread of normal cardiac excitation. They require larger than "physiologic" intercellular conductivities in order to make up for a lack of "anatomical" spatial scaling. Multicellular models for more in-depth quantitative studies will require more realistic anatomico-physiologic properties. (J Cardiovasc Electrophysiol, Vol. 14, pp. S121-S132, October 2003, Suppl.) [source] Temperature-sensitive TREK currents contribute to setting the resting membrane potential in embryonic atrial myocytesTHE JOURNAL OF PHYSIOLOGY, Issue 15 2008Hengtao Zhang TREK channels belong to the superfamily of two-pore-domain K+ channels and are activated by membrane stretch, arachidonic acid, volatile anaesthetics and heat. TREK-1 is highly expressed in the atrium of the adult heart. In this study, we investigated the role of TREK-1 and TREK-2 channels in regulating the resting membrane potential (RMP) of isolated chicken embryonic cardiac myocytes. At room temperature, the average RMP of embryonic day (ED) 11 atrial myocytes was ,22 ± 2 mV. Raising the temperature to 35°C hyperpolarized the membrane to ,69 ± 2 mV and activated a large outwardly rectifying K+ current that was relatively insensitive to conventional K+ channel inhibitors (TEA, 4-AP and Ba2+) but completely inhibited by tetracaine (200 ,m), an inhibitor of TREK channels. The heat-induced hyperpolarization was mimicked by 10 ,m arachidonic acid, an agonist of TREK channels. There was little or no inwardly rectifying K+ current (IK1) in the ED11 atrial cells. In marked contrast, ED11 ventricular myocytes exhibited a normal RMP (,86.1 ± 3.4 mV) and substantial IK1, but no temperature- or tetracaine-sensitive K+ currents. Both RT-PCR and real-time PCR further demonstrated that TREK-1 and TREK-2 are highly and almost equally expressed in ED11 atrium but much less expressed in ED11 ventricle. In addition, immunofluorescence demonstrated TREK-1 protein in the membrane of atrial myocytes. These data indicate the presence and function of TREK-1 and TREK-2 in the embryonic atrium. Moreover, we demonstrate that TREK-like currents have an essential role in determining membrane potential in embryonic atrial myocytes, where IK1 is absent. [source] Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1THE JOURNAL OF PHYSIOLOGY, Issue 3 2004Ron Bouchard The mechanisms underlying the inotropic effect of reductions in [K+]o were studied using recordings of membrane potential, membrane current, cell shortening and [Ca2+]i in single, isolated cardiac myocytes. Three types of mammalian myocytes were chosen, based on differences in the current density and intrinsic voltage dependence of the inwardly rectifying background K+ current IK1 in each cell type. Rabbit ventricular myocytes had a relatively large IK1 with a prominent negative slope conductance whereas rabbit atrial cells expressed much smaller IK1, with little or no negative slope conductance. IK1 in rat ventricle was intermediate in both current density and slope conductance. Action potential duration is relatively short in both rabbit atrial and rat ventricular myocytes, and consequently both cell types spend much of the duty cycle at or near the resting membrane potential. Rapid increases or decreases of [K+]o elicited significantly different inotropic effects in rat and rabbit atrial and ventricular myocytes. Voltage-clamp and current-clamp experiments showed that the effects on cell shortening and [Ca2+]i following changes in [K+]o were primarily the result of the effects of alterations in IK1, which changed resting membrane potential and action potential waveform. This in turn differentially altered the balance of Ca2+ efflux via the sarcolemmal Na+,Ca2+ exchanger, Ca2+ influx via voltage-dependant Ca2+ channels and sarcoplasmic reticulum (SR) Ca2+ release in each cell type. These results support the hypothesis that the inotropic effect of alterations of [K+]o in the heart is due to significant non-linear changes in the current,voltage relation for IK1 and the resulting modulation of the resting membrane potential and action potential waveform. [source] Electrophysiological effects of 5-hydroxytryptamine on isolated human atrial myocytes, and the influence of chronic , -adrenoceptor blockadeBRITISH JOURNAL OF PHARMACOLOGY, Issue 8 2003Davide Pau 5-Hydroxytryptamine (5-HT) has been postulated to play a proarrhythmic role in the human atria via stimulation of 5-HT4 receptors. The aims of this study were to examine the effects of 5-HT on the L-type Ca2+ current (ICaL) action potential duration (APD), the effective refractory period (ERP) and arrhythmic activity in human atrial cells, and to assess the effects of prior treatment with , -adrenoceptor antagonists. Isolated myocytes, from the right atrial appendage of 27 consenting patients undergoing cardiac surgery who were in sinus rhythm, were studied using the whole-cell perforated patch-clamp technique at 37°C. 5-HT (1 nM,10 ,M) caused a concentration-dependent increase in ICaL, which was potentiated in cells from , -blocked (maximum response to 5-HT, Emax=299±12% increase above control) compared to non- , -blocked patients (Emax=220±6%, P<0.05), but with no change in either the potency (log EC50: ,7.09±0.07 vs ,7.26±0.06) or Hill coefficient (nH: 1.5±0.6 vs 1.5±0.3) of the 5-HT concentration,response curve. 5-HT (10 ,M) produced a greater increase in the APD at 50% repolarisation (APD50) in cells from , -blocked patients (of 37±10 ms, i.e. 589±197%) vs non- , -blocked patients (of 10±4 ms, i.e. 157±54%; P<0.05). Both the APD90 and the ERP were unaffected by 5-HT. Arrhythmic activity was observed in response to 5-HT in five of 17 cells (29%) studied from , -blocked, compared to zero of 16 cells from the non- , -blocked patients (P<0.05). In summary, the 5-HT-induced increase in calcium current was associated with a prolonged early plateau phase of repolarisation, but not late repolarisation or refractoriness, and the enhancement of these effects by chronic , -adrenoceptor blockade was associated with arrhythmic potential. British Journal of Pharmacology (2003) 140, 1434,1441. doi:10.1038/sj.bjp.0705553 [source] Atrial Tachyarrhythmias Induced By Acetylcholine In Tilapia (Oreochromis SP.) Isolated AtriaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000Tsai-Chu Lin SUMMARY 1. Effects of the parasympathetic neuromediator acetylcholine (ACh) on atrial tissues vary greatly depending on the species, the type of atrial cells and experimental conditions. The aim of the present study was to investigate, with microelectrode techniques, the arrhythmogenic effects of ACh in tilapia (Oreochromis sp.) isolated atria at room (22,25°C) and high temperature (37°C). 2. Acetylcholine (1,10 ,mol/L) shortened action potential duration (APD), depressed action potential plateau and decreased twitch force in tilapia atria, as it did in human atrial fibres. In addition, ACh induced premature responses and re-entrant tachyarrhythmias (TA; frequency range from 7 to 25 Hz) in five of 19 and 14 of 22 tilapia atria tested at room and high temperature, respectively. The higher incidence of ACh-induced TA at 37°C compared with room temperature was statistically significant. 3. The ACh-induced TA consisted of high-frequency and uniform action potentials accompanied by tension oscillation and elevation of diastolic force (flutter). Acetylcholine-induced TA could be readily abolished by atropine (1 ,mol/L) and prevented by treatment with agents with local anaesthetic properties, such as 0.1 ,mol/L tetrodotoxin or 3 ,mol/L quinidine. The antagonistic action of quinidine occurred without significant prolongation of APD. 4. The present findings suggest that pharmacological concentrations of the cholinergic muscarinic agonist ACh readily induce TA (mainly atrial flutter) in tilapia atria, presumably via sodium channel-dependent re-entrant excitation. The poikilothermic tilapia appears to be an appropriate animal model for the study of atrial TA. [source] | |||||||||||||