成年大鼠心房肌牵张激活钾通道的牵张敏感性和门控机制

目的探讨成年大鼠心房肌细胞牵张激活钾通道（stretch-activated K+-selective channels,SAKCs）的电生理学特性,确定皮质细胞骨架在通道门控机制中的作用,对从通道水平阐明机械-电反馈具有重要的理论和实际意义。方法联合应用单通道膜片钳技术和压力钳技术,在急性分离的成年大鼠心房肌细胞上,采用细胞贴附（cell-atta-ched）方式记录SAKCs的活动。结果实验所记录的通道为SAKCs,通道闪烁样开放,无整流特性。当细胞外液为高K+液（140mmol/L）时,翻转电位为0mV。钳制膜电位+60mV时单通道的电导值为（59±5）pS,-60mV时为（51±8）pS。通道约在负压刺激开始700800ms内被快速激活,刺激解除后,通道快速在500ms内去激活。超过-30mmHg（1mmHg=0.133kPa）的刺激可使多个通道同时开放。实验中未观察到通道活动达到饱和现象。单通道电流幅度不受负压刺激的影响。随膜片钳电极内负压的增加,通道开放概率增大,呈刺激强度依赖性。Cytocha-lasin B不改变SAKCs的电流幅度,但增加SAKCs的开放概率,增强SAKCs的背景活动和对机械刺激的敏感性。结论我们推测生理状态下细胞皮质肌动蛋白内衬于细胞膜,可能作为细胞膜的并联成分承受部分细胞应力,并使脂质膜的应力减少,从而使SAKCs不易被激活。     

不同形态的家兔房室结细胞超极化钳制电流特性的研究

为探讨家兔房室结 3层细胞束细胞的电生理特性 ,按房室结 3层细胞束 4种细胞的形态特点 ,用胶原酶灌注分离房室结细胞并从中筛选 4种形态细胞 :圆形、椭圆形、细长形和条状形细胞 ,应用膜片钳全细胞记录技术观察各形房室结细胞超极化钳制电流的特征。超极化钳制时 ,房室结细胞中 12个条状形细胞中有 4个记录到较弱的内向整流钾电流 (Ik1 ) ,其他各形细胞均未记录到 Ik1 。大部分圆形和椭圆形细胞 (11 14 )记录到起搏电流 If,其电流密度为 - 4 .73± 0 .81p Ap F- 1 ,部分细长形细胞 (4 11)记录到较弱的 If,其电流密度为 - 0 .2 8± 0 .0 7p Ap F- 1 ,负向电流明显低于圆形和椭圆形细胞 (P<0 .0 1) ,长条形细胞除 1个外其余均未记录到 If。结果表明家兔房室结的 4种形态细胞的超极化钳制电流有明显不同 ,提示家兔房室结 3层细胞束的电生理及传导功能存在差异。     

不同形态的家兔房室结细胞超极化钳制电流特性的 …

为探讨家兔房室结３层细胞束细胞的电生理特性，按房室结３层细胞束４种细胞的形态特点，用胶原酶灌注分离房室结细胞并从中筛选４种形态细胞；圆形，椭圆形，细长形和条状形细胞，应用膜片钳全细胞记录技术观察各形房室结细胞超极化钳制电流的特征。超极化钳制时，房室结细胞中１２个条状形细胞中４个记录到较弱的内向整流钾电流（Ｉｋ１）其他各形细胞均未记录到Ｉｋ１。大部分圆形和椭圆形细胞（１１／１４）记录到起搏电流Ｉｆ，     

正常肠系膜动脉平滑肌细胞钙激活钾通道活性的观察

为了解人体正常肠系膜动脉平滑肌细胞钙激活钾通道的特性 ,取 2 4例人体正常肠系膜动脉小枝节段 ,用酶消化法获取标本细胞 ,以膜片钳制技术检测钙激活钾通道的活性 ,通过Pclamp专用软件实时采样记录其平均开放时间、平均关闭时间及平均开放概率等。结果发现 ,人体肠系膜动脉平滑肌细胞钙激活钾通道开放具有明显电压依赖性 ,在对称性高钾液中 ,电流 -电压关系曲线在 10～ 6 0mV范围内可被直线拟合。在细胞吸附式膜片和内面向外膜片中 ,通道电导分别为 192 .3± 2 9.2Ps和 2 0 2 .5± 5 8.3Ps。开放概率和开放数目随Ca2 + 浓度的增加而增加 ,膜内面应用四乙胺可减少通道开放概率及电流幅值。提示人体肠系膜动脉平滑肌细胞钙激活钾通道与人体其他血管相似 ,主要为大电导钙激活钾通道 ,具有电压和钙浓度双重依赖性。     

有氧运动抑制衰老大鼠脑动脉平滑肌STOC/BKCa功能下调

目的　探讨有氧运动训练对衰老大鼠脑动脉平滑肌细胞全细胞K⁺电流、自发瞬时外向电流及大电导钙激活钾通道生物物理特性的影响。方法　19～21月龄雄性Wistar大鼠12只（老年组）,随机分为安静组和有氧运动组,并选用2月龄Wistar大鼠安静处理作为青年对照组。12周后取脑动脉,急性分离动脉平滑肌细胞。分别采用膜片钳全细胞模式、穿孔膜片钳模式和单通道内面向外模式观察运动对全细胞K⁺电流、自发瞬时外向电流和大电导钙激活钾通道门控特性的影响。结果　安静组全细胞K⁺电流密度及对Iberiotoxin敏感性降低;安静组自发瞬时外向电流幅值降低,频率无明显变化;安静组大电导钙激活钾通道平均开放概率和平均开放时间显著低于青年对照组,而平均关闭时间高于青年对照组;电压依赖性和钙敏感性亦显著下降;与安静组相比,有氧运动可以增加全细胞K⁺电流密度、自发瞬时外向电流幅值及大电导钙激活钾通道平均开放概率、电压依赖性和钙敏感性来实现对大鼠脑动脉平滑肌自发瞬时外向电流/大电导钙激活钾通道功能的保护作用。结论　长期规律有氧运动可以减弱衰老所致的大鼠脑动脉平滑肌细胞大电导钙激活钾通道功能下调,这可能是有氧运动改善衰老动脉功能的重要机制之一。     

腺苷对心肌细胞的电生理作用及机制探讨

采用微电极技术及膜片钳全细胞记录方式，研究腺苷对豚鼠心肌细胞的电生理作用及其机制。结果表明：腺苷可明显缩短心房肌及房室结区细胞动作电位时程，降低房室结区细胞动作电位振幅、零相最大去极化速率，膜片钳上证明此为腺苷加强延迟整流性钾通道电流和抑制Ｌ型钙通道电流所致。对心室肌细胞无此明显的作用，但应用异丙肾上腺素后证明腺苷能拮抗β１受体的作用。腺苷的作用能被选择性腺苷Ａ１受体阻断剂８－环戊基－１，３－二丙基黄嘌呤消除，提示腺苷对心肌细胞的作用由Ａ１受体介导。本研究也探讨了腺苷对心房肌和心室肌作用区别的可能原因，以及心房肌和心室肌对异丙肾上腺素合用腺苷时反应不同的可能机制。     

线粒体三磷酸腺苷敏感性钾通道与心脑缺血

线粒体三磷酸腺苷 (ATP)敏感性钾 (mi toKATP)通道由Inoue等 ( 1 991年 )在小鼠肝脏细胞中发现。在随后开展的实验中 ,科学家们将研究扩展到了心脏、脑、胰腺等组织并发现开放mitoKATP通道与心脑抗缺血保护作用密切相关。本文拟对mitoKATP通道的特性、分子结构、开放机制及开放此通道后对心脑缺血的保护机制作一阐述。1　mitoKATP通道的生物学特征1 .1 　mitoKATP通道的特性和分子结构Inoue等在大鼠肝细胞中以膜片钳技术发现 ,在线粒体内有一种对K+高度敏感的通道 ,当线粒体基质ATP不足时 ,此通道开放 ,线粒体产生内向K+电流而…     

大鼠心房肌细胞三磷酸腺苷敏感钾通道的牵张敏感性

目的研究成年大鼠心房肌细胞三磷酸腺苷敏感钾通道(KATP)的牵张敏感性。方法应用单通道膜片钳技术在开放细胞贴附模式下记录大鼠心房肌细胞上KATP通道的电活动,并研究KATP通道对机械刺激的反应。结果根据通道的激活方式、药理学特性、I-V曲线、反转电位及整流特性,确定所记录的通道为KATP通道。进一步研究表明该通道的开放概率对负压刺激呈现强度依赖性。结论大鼠心房肌细胞上的KATP通道对牵张刺激敏感。     

灯盏花素对鼠主动脉平滑肌钙激活钾通道的激活作用

目的:观察灯盏花素对大鼠主动脉平滑肌钙激活钾通道(KCa)的影响,揭示灯盏花素在分子水平的作用机制。方法:采用Wistar大鼠20只,应用膜片钳技术,研究灯盏花素对大鼠主动脉平滑肌KCa的作用。结果:细胞贴附式膜片上,应用浓度分别为5×10-4、10-3、1.85×10-3mol/L的灯盏花素后,大鼠的通道开放概率(Po)及通道电导明显增大:Po分别由用药前的0.012±0.047增加至0.427±0.364,0.609±0.312(P<0.05),0.839±0.192(P<0.01);通道电导分别由用药前的(124±59)pS增大至(174±83)pS,(199±41)pS(P<0.05),(269±85)pS(P<0.01)。结论:灯盏花素可激活KCa,从而起到舒张血管的作用。     

甲状腺素诱发大鼠心肌肥厚时瞬时外向钾电流、内向整流钾电流和钙电流的变化

目的 研究甲状腺素诱发大鼠心肌肥厚模型的心肌细瞬时外向钾电流、内向整流钾电流和钙电流的变化。方法 以ipL-甲门面腺素造成大鼠心肌肥厚模型后,用膜片钳技术记录心肌细胞瞬时外向钾电流、内向整流钾电流和L型钙电流。结果 肥厚组心肌细胞瞬时外向钾电流幅度和心坎产增加,激活动力学特性无改变;内向整流钾电流幅度和密度也增加,激活动力学特性也无改变;而钙电流幅度、细胞膜电容增加,电流密度不变,半数激活电压（V1/2）向负电位方向移动,斜率（k)减小。结论 在甲状腺素诱发大鼠心肌肥厚模型中瞬时外向钾电流、内向整流钾电流和钙电流特性均发生了变化,这是造成肥厚心肌电生理异常的离子基础。     

Hyperkalemia enhances the effect of adenosine on IK,ADO in rabbit isolated AV nodal myocytes and on AV nodal conduction in guinea pig isolated heart

BACKGROUND: The atrioventricular (AV) node is insensitive to changes in extracellular potassium concentration, [K+]o, because of the absence of the inward rectifier potassium current (IK1). However, we propose that in the presence of adenosine, elevated [K+]o should increase the adenosine-activated inward rectifier potassium current (IK,ADO) in AV nodal myocytes and hence augment the negative dromotropic effect of the nucleoside. METHODS AND RESULTS: The effects of normal (4.8 mmol/L) and high (8.0 mmol/L) [K+]o on adenosine-induced changes in resting membrane potential (Vm), IK,ADO, and membrane resistance (Rm) in rabbit isolated AV nodal myocytes and in AV nodal conduction delay (atrium-to-His bundle, AH, interval) in guinea pig isolated hearts were determined with the use of whole-cell patch-clamp and His bundle electrogram techniques, respectively. High [K+]o alone did not significantly affect membrane current, Rm, or Vm in AV nodal myocytes. However, high [K+]o in the presence of adenosine (3 micromol/L) markedly increased Im (-0. 249+/-0.038 to -0.571+/-0.111 nA, P<0.05) at -100 mV and reduced Rm (151+/-21 to 77+/-8 MOmega, P<0.02). Adenosine still hyperpolarized Vm from -48+/-2 to -65+/-1 mV (P<0.001). High [K+]o alone did not significantly affect the AH interval in isolated hearts. However, high [K+]o markedly lengthened the AH interval prolongation caused by adenosine (4 micromol/L, 7.9+/-0.8 vs 22.1+/-3.0 ms, P<0.001). The potentiating effect of high [K+]o on adenosine-induced delay in AV nodal conduction was abolished by BaCl2 (100 micromol/L). CONCLUSIONS: By increasing IK,ADO and decreasing Rm of AV nodal myocytes, elevated [K+]o, augments the depressant effect of adenosine on AV nodal conduction.     

Adenosine-activated potassium conductance in cultured striatal neurons.

We have examined the effect of adenosine on the membrane properties of cultured embryonic mouse striatal neurons using patch electrode techniques. Adenosine at 50 microM effectively blocked spontaneous action potential activity. Adenosine or 2-chloroadenosine caused a slow hyperpolarization of the membrane potential and, under voltage clamp, an outward current that was blocked by 1 mM theophylline. ATP also caused a hyperpolarization that was slower and weaker than the adenosine response and could be blocked by 1 mM theophylline. The current induced by adenosine appears to be carried by potassium since (i) an inward current was generated by adenosine when the cells were internally perfused with cesium salts and (ii) the reversal potential of the outward current shifted 57 mV with a 10-fold change in extracellular potassium concentration. The adenosine response is voltage dependent in that the current evoked by adenosine is reduced at holding potentials more positive than -55 mV, despite a larger driving force. Though calcium influx is not required for adenosine to activate the potassium conductance, some components of the cytosol may be essential, since the response is lost during intracellular perfusion.     

Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia

Long RP' supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP' SVT (RP'/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 micrograms/kg), which increases potassium current (iK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (-90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K+ current likely comprise depressed fast-Na+ channel tissue, i.e., partially depolarized (greater than -60 to -70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K+ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of -60 mV or less.     

Ethanol Increases K+ Conductance in Human T-Cells

Ethanol increased the open probability of a K channel in cultured human T-cells. Single-channel currents were studied using the patch-clamp technique in cell-attached configuration. Ethanol increased the number of simultaneously active channels and subsequent current maxima at concentrations of 35 and 50 mM from control levels of 3.2 to 4.6 pA and 8.4 PA, respectively. Current responses were elicited by a 80 mV hyperpolarizing pulse following adjustment to the same resting potential. The channel was K-selective as determined by the reversal potentials under different Na-K gradients. When the pipette contained 155 mM K, single-channel currents had a slope conductance of 28 pS and a reversal potential of -4.3 mV. Baseline current levels often shifted in a negative direction during the application of ethanol, indicating a hyperpolarization of the membrane potential and an increase in channel activity.     

Ionic basis for the antagonism between adenosine and isoproterenol on isolated mammalian ventricular myocytes

We studied the effects of adenosine and isoproterenol on membrane currents of isolated bovine and guinea pig ventricular myocytes with a two-microelectrode voltage clamp technique. Adenosine (50 microM to 0.2 mM) alone had no effect on any of the membrane currents measured, but it antagonized the effects induced by 10 nM isoproterenol. Peak calcium membrane current was augmented by isoproterenol from a control of 4.8 +/- 0.6 to 8.6 +/- 0.8 nA and adenosine reduced it to 5.7 +/- 0.7 nA (mean +/- SEM of six cells). The inactivation time constant was not altered by isoproterenol alone or isoproterenol plus adenosine, and neither was the voltage dependence of peak calcium membrane current. Thus, the changes caused by isoproterenol could be described as an increase in maximal calcium conductance from 0.86 +/- 0.7 to 1.55 +/- 0.04 mS/cm2 and partially antagonized by adenosine to 0.97 +/- 0.04 mS/cm2. Isoproterenol also increased the non-inactivating component of calcium membrane current from 17 +/- 1 to 24 +/- 4%, and adenosine reduced it to 18 +/- 2% (n = 4). The steady state activation and inactivation variables remained unchanged. Consistent with these effects on calcium membrane current, adenosine completely antagonized the isoproterenol-induced increase of the slow action potentials obtained in sodium-free medium. Isoproterenol increased the steady state outward currents at potentials between -90 and -30 mV (i.e., probable iK1). Adenosine alone had no effect on potassium membrane current, but it antagonized the effects of isoproterenol. Slow action potentials in 25 mM potassium were enhanced by isoproterenol, but were only moderately attenuated by adenosine. Accordingly, in 25 mM potassium the isoproterenol-induced changes in membrane currents were not antagonized by adenosine. This lack of inhibition by adenosine of the isoproterenol effects in 25 mM potassium could not be mimicked by 1-minute-long conditioning prepulses to -45 mV. The results indicate that adenosine by itself (absence of isoproterenol) has no effect on maximal calcium conductance, that the isoproterenol-induced increase in cyclic adenosine 3',5'-monophosphate, which leads to an increase in maximal calcium conductance, is antagonized by adenosine, and that such action can account for the ability of adenosine to attenuate the stimulatory effects of isoproterenol.     

Hyposmotic membrane stretch potentiated muscarinic receptor agonist—induced depolarization of membrane potential in guinea—pig gastric myocytes

AIM：To investigate the relationship between hyposmotic membrane stretch and muscarinic receptor agonist-induced depolarization of membrane potential in antral gastric circular myocytes of guinea-pig.METHODS:Using whole cell patch-clamp technique recorded membrane potential and current in single gastric myocytes isolated by collagenase.RESULTS:Hyposmotic membrane stretchhyperpolarized membrane potential from-60.0mV&#177;1.0mVto-67.9mV&#177;1.0mV,TEA(10mmol/L),a nonselective potassium channel blocker significantly inhibitea hyposmotic membrane stretch-induced hyperpolarization.After KCI in the pipette and NaCl in the external solution were replaced by CsCI to block the potassium current,hyposmotic membrane stretch depolarized the membrane potential from-60.0mV&#177;1.0mVto-44.8mV&#177;2.3mV(P&lt;0.05).and atropine(1μmol/L）inhibited the depolarization of the membrane potential.Muscarinic receptor agonist Carbachol depolarized membrane potential from-60.0mV&#177;1.0mVto-50.3mV&#177;0.3mV(P&lt;0.05)and hyposmotic membrane stretch potentiated the depolarization.Carbachol induced muscarinic current(Icch)was greatly increased by hyposmotic membrane stretch.CONCLUSION:Hyposmotic membrane stretch potentiated muscarinic receptor agonist-induced depolarization of membrane potential,which is related to hyposmotic membrane stretch-induced increase of muscarinic current.     

Role of calcium-activated potassium currents in CNP-induced relaxation of gastric antral circular smooth muscle in guinea pigs

AIM: To investigate ion channel mechanism in CNP-induced relaxation of gastric circular smooth muscle in guinea pigs.METHODS: Spontaneous contraction of gastric smooth muscle was recorded by a four -channel physiograph. The whole cell patch-damp technique was used bo record calcium-activated potassium currents and membrane potential in the gastric myocytes isolated by collagenase.RESULTS: C-type natriuretic peptide (CNP) markedly inhibited the spontaneous contraction in a dose-dependent manner in gastric circular smooth muscle in guinea pigs.Ly83583, an inhibitor of guanylate cyclase, weakened CNP-induced inhibition on spontaneous contraction but Zaparinast, an inhibitor of cGMP sensitive phosphoesterase,potentiated CNP-induced inhibition in gastric circular smooth muscles. The inhibitory effects of CNP on spontaneous contraction were blocked by tetrathylammonium (TEA), a nonselective potassium channel blocker. CNP hyperpolarized membrane potential from -60.0 mV&#177;2.0 mV to -68.3 mV&#177;3.0 mV in a single gastric myocyte. CNP increased calcium-activated potassium currents (IK（ca)) in a dose-dependent manner in gastric circular myocytes. CNP also increased the spontaneously transient outward currents(STOCs). Ly83583 partly blocked CNP-induced increase of calcium-activated potassium currents, but Zaparinast potented the effect.CONCLUSION:CNP inhibits spontaneous contraction,and potassium channel may be involved in the process in gastric circular smooth muscle of guinea pigs.CNP-induced increase of IK(ca) mediated by a cGMP dependent pathway.     

Ionic basis of a differential effect of adenosine on refractoriness in rabbit AV nodal and atrial isolated myocytes

OBJECTIVES: Firstly, to compare effects of adenosine on membrane potential and refractoriness in AV nodal and atrial cells. Secondly, to assess the contribution of the effects of adenosine on IKAdo and ICaL to its effects on the functional electrophysiological properties in the two cell types. METHODS: The whole cell patch clamp technique was used to record action potentials and ion currents in AV nodal and left atrial myocytes isolated enzymatically from rabbit hearts. RESULTS: Adenosine (10 microM) caused similar hyperpolarisation and shortening of the action potential duration (APD) in both cell types: maximum diastolic potential was hyperpolarised from -59 +/- 3 to -66 +/- 2 and from -70 +/- 2 to -76 +/- 2 mV (mean +/- SEM) and APD90 was shortened by 31 +/- 4 and 30 +/- 7% in AV nodal (n = 14) and atrial cells (n = 8), respectively. Adenosine shortened the effective refractory period (ERP) in atrial cells, from 124 +/- 15 to 98 +/- 14 ms (n = 8). In contrast, ERP in AV nodal cells was not significantly affected (112 +/- 13 vs. 102 +/- 12 ms, n = 14), and post-repolarization refractoriness was prolonged. By contrast, current injection, to induce an equal degree of hyperpolarisation to that produced by adenosine, shortened APD and ERP in both cell types, suggesting an additional action of adenosine in AV nodal cells. Adenosine (10 microM) did not affect peak ICaL in AV nodal cells, but significantly altered the biexponential time course of recovery of ICaL from inactivation. The proportion of recovery in the fast phase (time constant, tau = 102 +/- 10 ms) was reduced from 71 +/- 3 to 55 +/- 5%, with shift to the slow phase (tau = 858 +/- 168 ms), without altering tau in either phase. A similar effect of adenosine was seen in left atrial cells. CONCLUSION: Adenosine caused hyperpolarisation, APD-shortening and slowing of recovery of ICaL from inactivation, in both AV nodal and atrial cells, but prolonged post-repolarisation refractoriness in AV nodal cells only. This differential effect of adenosine on refractoriness in the two cell types could not be explained by effects on IKAdo, but may be due to slowed reactivation of ICaL, which is the predominant inward current in AV nodal but not left atrial cells.     

An inward rectifier and a voltage-dependent K+ current in single, cultured pericytes from bovine heart

OBJECTIVE: The purpose of this study was to describe passive electrical properties and major membrane currents in coronary pericytes. METHODS: 78 single, cultured bovine pericytes were studied with the patch-clamp technique in the whole-cell mode. RESULTS: The membrane potential of the cells was -48.9+/-9.6 mV (mean+/-S.D.) with 5 mM and -23.2+/-2.2 mV with 60 mM extracellular K+. The membrane capacitance was 150.2+/-123.2 pF. The current-voltage relation of the pericytes was dominated by an inward current at hyperpolarized potentials and an outward current at depolarized potentials. Increasing extracellular K+ from 5 to 60 mM led to an increase of the inward current and to a shift of this current to more depolarized potentials. The inward current was very sensitive to extracellular barium (50 microM). The maximum slope conductance of the cells at hyperpolarized potentials was 2.9+/-2.8 nS. Inward rectification of whole-cell currents was steep (slope factor = 6.8 mV). With elevated external K+ the outward current reversed near the potassium equilibrium potential. Onset of the outward current was sigmoid and inactivation of this current was monoexponential, slow (time constant = 12.8 s) and incomplete. Voltage-dependence of outward current steady-state activation was steep (slope factor = 4.6 mV). The outward current was very sensitive to 4-aminopyridine (dissociation constant = 0.1 mM). The maximum slope conductance at depolarized potentials was 16.6+/-15.6 nS. CONCLUSION: We report for the first time, patch-clamp recordings from coronary pericytes. An inward rectifier and a voltage-dependent K+ current were identified and characterized. Regulation of these currents may influence coronary blood flow.     

Adenosine and its cardiovascular effects.

Adenosine is a new antiarrhythmic agent recently released with the permission of the Food and Drug Administration. It is an endogenously occurring nucleoside indicated for use in the diagnosis and treatment of supraventricular tachycardia. Its greatest utility is in patients with AV nodal reentry. Its antiarrhythmic action is mediated at the cellular level through the potassium channel, causing hyperpolarization of the myocyte membrane potential. In addition to its current indication as an antiarrhythmic agent, adenosine is now being used under an investigational protocol for pharmacologic stress testing. It can be given in conjunction with thallium or used in echocardiography as an imaging tool for patients who can not be adequately exercised. Adenosine's side effect profile is relatively benign and the agent's extremely short half-life makes most adverse reactions clinically insignificant. In this report we attempt to highlight this agent's clinical utility and discuss its future in the cardiovascular pharmacopeia.