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Published: 4 June 2021

Last updated: 10 February 2022

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1

Magee, William P., Gayatri Deshmukh, Michael P. Deninno, Jill C. Sutt, Justin G. Chapman, and W. Ross Tracey. "Differing cardioprotective efficacy of the Na+/Ca2+ exchanger inhibitors SEA0400 and KB-R7943." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H903—H910. http://dx.doi.org/10.1152/ajpheart.00784.2002.

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KB-R7943 and SEA0400 are Na+/Ca2+ exchanger (NCX) inhibitors with differing potency and selectivity. The cardioprotective efficacy of these NCX inhibitors was examined in isolated rabbit hearts (Langendorff perfused) subjected to regional ischemia (coronary artery ligation) and reperfusion. KB-R7943 and SEA0400 elicited concentration-dependent reductions in infarct size (SEA0400 EC50: 5.7 nM). SEA0400 was more efficacious than KB-R7943 (reduction in infarct size at 1 μM: SEA0400, 75%; KB-R7943, 40%). Treatment with either inhibitor yielded similar reductions in infarct size whether administered before or after regional ischemia. SEA0400 (1 μM) improved postischemic recovery of function (±dP/d t), whereas KB-R7943 impaired cardiac function at ≥1 μM. At 5–20 μM, KBR-7943 elicited rapid and profound depressions of heart rate, left ventricular developed pressure, and ±dP/d t. Thus the ability of KB-R7943 to provide cardioprotection is modest and limited by negative effects on cardiac function, whereas the more selective NCX inhibitor SEA0400 elicits marked reductions in myocardial ischemic injury and improved ±dP/d t. NCX inhibition represents an attractive approach for achieving clinical cardioprotection.

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2

Elias, Chadwick L., Anton Lukas, Sabin Shurraw, Jason Scott, Alexander Omelchenko, Gil J. Gross, Mark Hnatowich, and Larry V. Hryshko. "Inhibition of Na+/Ca2+ exchange by KB-R7943: transport mode selectivity and antiarrhythmic consequences." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (September 1, 2001): H1334—H1345. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1334.

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The Na+/Ca2+ exchanger plays a prominent role in regulating intracellular Ca2+ levels in cardiac myocytes and can serve as both a Ca2+ influx and efflux pathway. A novel inhibitor, KB-R7943, has been reported to selectively inhibit the reverse mode (i.e. , Ca2+ entry) of Na+/Ca2+ exchange transport, although many aspects of its inhibitory properties remain controversial. We evaluated the inhibitory effects of KB-R7943 on Na+/Ca2+exchange currents using the giant excised patch-clamp technique. Membrane patches were obtained from Xenopus laevis oocytes expressing the cloned cardiac Na+/Ca2+exchanger NCX1.1, and outward, inward, and combined inward-outward currents were studied. KB-R7943 preferentially inhibited outward (i.e., reverse) Na+/Ca2+ exchange currents. The inhibitory mechanism consists of direct effects on the transport machinery of the exchanger, with additional influences on ionic regulatory properties. Competitive interactions between KB-R7943 and the transported ions were not observed. The antiarrhythmic effects of KB-R7943 were then evaluated in an ischemia-reperfusion model of cardiac injury in Langendorff-perfused whole rabbit hearts using electrocardiography and measurements of left ventricular pressure. When 3 μM KB-R7943 was applied for 10 min before a 30-min global ischemic period, ventricular arrhythmias (tachycardia and fibrillation) associated with both ischemia and reperfusion were almost completely suppressed. The observed electrophysiological profile of KB-R7943 and its protective effects on ischemia-reperfusion-induced ventricular arrhythmias support the notion of a prominent role of Ca2+ entry via reverse Na+/Ca2+ exchange in this process.

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3

Chorro, Francisco J., Isabel Trapero, Luis Such-Miquel, Francisca Pelechano, Luis Mainar, Joaquín Cánoves, Álvaro Tormos, et al. "Pharmacological modifications of the stretch-induced effects on ventricular fibrillation in perfused rabbit hearts." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1860—H1869. http://dx.doi.org/10.1152/ajpheart.00144.2009.

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Stretch induces modifications in myocardial electrical and mechanical activity. Besides the effects of substances that block the stretch-activated channels, other substances could modulate the effects of stretch through different mechanisms that affect Ca2+ handling by myocytes. Thirty-six Langendorff-perfused rabbit hearts were used to analyze the effects of the Na+/Ca2+ exchanger blocker KB-R7943, propranolol, and the adenosine A2 receptor antagonist SCH-58261 on the acceleration of ventricular fibrillation (VF) produced by acute myocardial stretching. VF recordings were obtained with two epicardial multiple electrodes before, during, and after local stretching in four experimental series: control ( n = 9), KB-R7943 (1 μM, n = 9), propranolol (1 μM, n = 9), and SCH-58261 (1 μM, n = 9). Both the Na+/Ca2+ exchanger blocker KB-R7943 and propranolol induced a significant reduction ( P < 0.001 and P < 0.05, respectively) in the dominant frequency increments produced by stretching with respect to the control and SCH-58261 series (control = 49.9%, SCH-58261 = 52.1%, KB-R7943 = 9.5%, and propranolol = 12.5%). The median of the activation intervals, the functional refractory period, and the wavelength of the activation process during VF decreased significantly under stretch in the control and SCH-58261 series, whereas no significant variations were observed in the propranolol and KB-R7943 series, with the exception of a slight but significant decrease in the median of the fibrillation intervals in the KB-R7943 series. KB-R7943 and propranolol induced a significant reduction in the activation maps complexity increment produced by stretch with respect to the control and SCH-58261 series. In conclusion, the electrophysiological effects responsible for stretch-induced VF acceleration in the rabbit heart are reduced by the Na+/Ca2+ exchanger blocker KB-R7943 and by propranolol but not by the adenosine A2 receptor antagonist SCH-58261.

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4

Pezier, A., Y. V. Bobkov, and B. W. Ache. "The Na+/Ca2+ Exchanger Inhibitor, KB-R7943, Blocks a Nonselective Cation Channel Implicated in Chemosensory Transduction." Journal of Neurophysiology 101, no. 3 (March 2009): 1151–59. http://dx.doi.org/10.1152/jn.90903.2008.

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The mechanism(s) of olfactory transduction in invertebrates remains to be fully understood. In lobster olfactory receptor neurons (ORNs), a nonselective sodium-gated cation (SGC) channel, a presumptive transient receptor potential (TRP)C channel homolog, plays a crucial role in olfactory transduction, at least in part by amplifying the primary transduction current. To better determine the functional role of the channel, it is important to selectively block the channel independently of other elements of the transduction cascade, causing us to search for specific pharmacological blockers of the SGC channel. Given evidence that the Na+/Ca2+ exchange inhibitor, KB-R7943, blocks mammalian TRPC channels, we studied this probe as a potential blocker of the lobster SGC channel. KB-R7943 reversibly blocked the SGC current in both inside- and outside-out patch recordings in a dose- and voltage-dependent manner. KB-R7943 decreased the channel open probability without changing single channel amplitude. KB-R7943 also reversibly and in a dose-dependent manner inhibited both the odorant-evoked discharge of lobster ORNs and the odorant-evoked whole cell current. Our findings strongly imply that KB-R7943 potently blocks the lobster SGC channel and likely does so directly and not through its ability to block the Na+/Ca2+ exchanger.

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5

Yamamura, Hisao, William C. Cole, Satomi Kita, Shingo Hotta, Hidemichi Murata, Yoshiaki Suzuki, Susumu Ohya, Takahiro Iwamoto, and Yuji Imaizumi. "Overactive bladder mediated by accelerated Ca2+influx mode of Na+/Ca2+exchanger in smooth muscle." American Journal of Physiology-Cell Physiology 305, no. 3 (August 1, 2013): C299—C308. http://dx.doi.org/10.1152/ajpcell.00065.2013.

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The Na+/Ca2+exchanger (NCX) is thought to be a key molecule in the regulation of cytosolic Ca2+dynamics. The relative importance of the two Ca2+transport modes of NCX activity leading to Ca2+efflux (forward) and influx (reverse) in smooth muscle, however, remains unclear. Unexpectedly, spontaneous contractions of urinary bladder smooth muscle (UBSM) were enhanced in transgenic mice overexpressing NCX1.3 (NCX1.3tg/tg). The enhanced activity was attenuated by KB-R7943 or SN-6. Whole cell outward NCX current sensitive to KB-R7943 or Ni2+was readily detected in UBSM cells from NCX1.3tg/tgbut not wild-type mice. Spontaneous Ca2+transients in myocytes of NCX1.3tg/tgwere larger and frequently resulted in propagating events and global elevations in cytosolic Ca2+concentration. Significantly, NCX1.3tg/tgmice exhibited a pattern of more frequent urination of smaller volumes and this phenotype was reversed by oral administration of KB-R7943. On the other hand, KB-R7943 did not improve it in KB-R7943-insensitive (G833C-)NCX1.3tg/tgmice. We conclude that NCX1.3 overexpression is associated with abnormal urination owing to enhanced Ca2+influx via reverse mode NCX leading to prolonged, propagating spontaneous Ca2+release events and a potentiation of spontaneous UBSM contraction. These findings suggest the possibility that NCX is a candidate molecular target for overactive bladder therapy.

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6

Kim, Moon Young, Geun Hee Seol, Guo Hua Liang, Ji Aee Kim, and Suk Hyo Suh. "Na+-K+ pump activation inhibits endothelium-dependent relaxation by activating the forward mode of Na+/Ca2+ exchanger in mouse aorta." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H2020—H2029. http://dx.doi.org/10.1152/ajpheart.00908.2004.

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The effect of Na+-K+ pump activation on endothelium-dependent relaxation (EDR) and on intracellular Ca2+ concentration ([Ca2+]i) was examined in mouse aorta and mouse aortic endothelial cells (MAECs). The Na+-K+ pump was activated by increasing extracellular K+ concentration ([K+]o) from 6 to 12 mM. In aortic rings, the Na+ ionophore monensin evoked EDR, and this EDR was inhibited by the Na+/Ca2+ exchanger (NCX; reverse mode) inhibitor KB-R7943. Monensin-induced Na+ loading or extracellular Na+ depletion (Na+ replaced by Li+) increased [Ca2+]i in MAECs, and this increase was inhibited by KB-R7943. Na+-K+ pump activation inhibited EDR and [Ca2+]i increase (K+-induced inhibition of EDR and [Ca2+]i increase). The Na+-K+ pump inhibitor ouabain inhibited K+-induced inhibition of EDR. Monensin (>0.1 μM) and the NCX (forward and reverse mode) inhibitors 2′4′-dichlorobenzamil (>10 μM) or Ni2+ (>100 μM) inhibited K+-induced inhibition of EDR and [Ca2+]i increase. KB-R7943 did not inhibit K+-induced inhibition at up to 10 μM but did at 30 μM. In current-clamped MAECs, an increase in [K+]o from 6 to 12 mM depolarized the membrane potential, which was inhibited by ouabain, Ni2+, or KB-R7943. In aortic rings, the concentration of cGMP was significantly increased by acetylcholine and decreased on increasing [K+]o from 6 to 12 mM. This decrease in cGMP was significantly inhibited by pretreating with ouabain (100 μM), Ni2+ (300 μM), or KB-R7943 (30 μM). These results suggest that activation of the forward mode of NCX after Na+-K+ pump activation inhibits Ca2+ mobilization in endothelial cells, thereby modulating vasomotor tone.

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7

Saini, Harjot K., Onkar N. Tripathi, Shetuan Zhang, Vijayan Elimban, and Naranjan S. Dhalla. "Involvement of Na+/Ca2+ exchanger in catecholamine-induced increase in intracellular calcium in cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 1 (January 2006): H373—H380. http://dx.doi.org/10.1152/ajpheart.00613.2005.

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Although sarcolemmal (SL) Na+/Ca2+ exchanger is known to regulate the intracellular Ca2+ concentration ([Ca2+]i), its involvement in catecholamine-induced increase in [Ca2+]i is not fully understood. To gain some information in this regard, isolated rat cardiomyocytes were treated with different agents, which are known to modify Ca2+ movements, in the absence or presence of a β-adrenoceptor agonist, isoproterenol, and [Ca2+]i in cardiomyocytes was determined spectrofluorometrically with fura-2 AM. Treatment with isoproterenol did not alter [Ca2+]i in quiescent cardiomyocytes, whereas the ATP (purinergic receptor agonist)-induced increase in [Ca2+]i was significantly potentiated by isoproterenol. Unlike ryanodine and cyclopiazonic acid, which affect the sarcoplasmic reticulum function, SL L-type Ca2+ channel blockers verapamil and diltiazem, as well as a SL Ca2+-pump inhibitor, vanadate, caused a significant depression in the isoproterenol-induced increase in [Ca2+]i. The SL Na+/Ca2+ exchange blockers amiloride, Ni2+, and KB-R7943 also attenuated the isoproterenol-mediated increase in [Ca2+]i. Combination of KB-R7943 and verapamil showed additive inhibitory effects on the isoproterenol-induced increase in [Ca2+]i. The isoproterenol-induced increase in [Ca2+]i in KCl-depolarized cardiomyocytes was augmented by low Na+; this augmentation was significantly depressed by treatment with KB-R7943. The positive inotropic action of isoproterenol in isolated hearts was also reduced by KB-R7943. These data suggest that in addition to SL L-type Ca2+ channels, SL Na+/Ca2+ exchanger seems to play an important role in catecholamine-induced increase in [Ca2+]i in cardiomyocytes.

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8

Amran, Md Shah, Nobuo Homma, and Keitaro Hashimoto. "Pharmacology of KB-R7943: A Na+-Ca2+ exchange inhibitor." Cardiovascular Drug Reviews 21, no. 4 (June 7, 2006): 255–76. http://dx.doi.org/10.1111/j.1527-3466.2003.tb00121.x.

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9

Algara-Suárez, Paola, Catalina Romero-Méndez, Tom Chrones, Sergio Sánchez-Armass, Ulises Meza, Stephen M. Sims, and Ricardo Espinosa-Tanguma. "Functional coupling between the Na+/Ca2+ exchanger and nonselective cation channels during histamine stimulation in guinea pig tracheal smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L191—L198. http://dx.doi.org/10.1152/ajplung.00485.2006.

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Airway smooth muscle (ASM) contracts partly due to an increase in cytosolic Ca2+. In this work, we found that the contraction caused by histamine depends on external Na+, possibly involving nonselective cationic channels (NSCC) and the Na+/Ca2+ exchanger (NCX). We performed various protocols using isometric force measurement of guinea pig tracheal rings stimulated by histamine. We observed that force reached 53 ± 1% of control during external Na+ substitution by N-methyl-d-glucamine+, whereas substitution by Li+ led to no significant change (91 ± 1%). Preincubation with KB-R7943 decreased the maximal force developed (52.3 ± 5.6%), whereas preincubation with nifedipine did not (89.7 ± 1.8%). Also, application of the nonspecific NCX blocker KB-R7943 and nifedipine on histamine-precontracted tracheal rings reduced force to 1 ± 3%, significantly different from nifedipine alone (49 ± 6%). Moreover, nonspecific NSCC inhibitors SKF-96365 and 2-aminoethyldiphenyl borate reduced force to 1 ± 1% and 19 ± 7%, respectively. Intracellular Ca2+ measurements in isolated ASM cells showed that KB-R7943 and SKF-96365 reduced the peak and sustained response to histamine (0.20 ± 0.1 and 0.19 ± 0.09 for KB-R, 0.43 ± 0.16 and 0.47 ± 0.18 for SKF, expressed as mean of differences). Moreover, Na+-free solution only inhibited the sustained response (0.54 ± 0.25). These data support an important role for NSCC and NCX during histamine stimulation. We speculate that histamine induces Na+ influx through NSCC that promotes the Ca2+ entry mode of NCX and CaV1.2 channel activation, thereby causing contraction.

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10

Huang, Jingbo, Leif Hove-Madsen, and Glen F. Tibbits. "SR Ca2+ refilling upon depletion and SR Ca2+ uptake rates during development in rabbit ventricular myocytes." American Journal of Physiology-Cell Physiology 293, no. 6 (December 2007): C1906—C1915. http://dx.doi.org/10.1152/ajpcell.00241.2007.

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While it has been reported that a sparse sarcoplasmic reticulum (SR) and a low SR Ca2+ pump density exist at birth, we and others have recently shown that significant amounts of Ca2+ are stored in the neonatal rabbit heart SR. Here we try to determine developmental changes in SR Ca2+ loading mechanisms and Ca2+ pump efficacy in rabbit ventricular myocytes. SR Ca2+ loading (loadSR) and k0.5 (Ca2+ concentration at half-maximal SR Ca2+ uptake) were higher and lower, respectively, in younger age groups. Inhibition of the L-type calcium current ( ICa) with 15 μM nifedipine dramatically reduced loadSR in older but not in younger age groups. In contrast, subsequent inhibition of the Na+/Ca2+ exchanger (NCX) with 10 μM KB-R7943 strongly reduced loadSR in the younger but not the older age groups. Accordingly, the time integral of the inward NCX current (tail INCX) elicited on repolarization was highly sensitive to nifedipine in the older groups and sensitive to KB-R7943 in the younger groups. Interestingly, slow SR loading took place in the presence of both nifedipine and KB-R7943 in all age groups, although it was less prominent in the older groups. We conclude that the SR loading capacity at the earliest postnatal stages is at least as large as that of adult myocytes. However, reverse-mode NCX plays a prominent role in SR Ca2+ loading at early postnatal stages while ICa is the main source of SR Ca2+ loading at late postnatal and adult stages.

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11

Weiss, Michael, Myoungki Baek, and Wonku Kang. "Systems analysis of digoxin kinetics and inotropic response in the rat heart: effects of calcium and KB-R7943." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (October 2004): H1857—H1867. http://dx.doi.org/10.1152/ajpheart.01121.2003.

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To gain more insight into the mechanistic processes controlling the kinetics of inotropic response of digoxin in the perfused whole heart, an integrated kinetic model was developed incorporating digoxin uptake, receptor binding (Na+-K+-ATPase inhibition), and cellular events linking receptor occupation and response. The model was applied to data obtained in the single-pass Langendorff-perfused rat heart for external [Ca2+] of 0.5 and 1.5 mM under control conditions and in the presence of the reverse-mode Na+/Ca2+ exchange inhibitor KB-R7943 (0.1 μM) in perfusate. Outflow concentration and left ventricular developed pressure data measured for three consecutive doses (15, 30, and 45 μg) in each heart were analyzed simultaneously. While disposition kinetics of digoxin was determined by interaction with a heterogeneous receptor population consisting of a high-affinity/low-capacity and a low-affinity/high- capacity binding site, response generation was >80% mediated by binding to the high-affinity receptor. Digoxin sensitivity increased at lower external [Ca2+] due to higher stimulus amplification. Coadministration of KB-R7943 significantly reduced the positive inotropic effect of digoxin at higher doses (30 and 45 μg) and led to a saturated and delayed receptor occupancy-response relationship in the cellular effectuation model. The results provide further evidence for the functional heterogeneity of the Na+-K+-ATPase and suggest that in the presence of KB-R7943 a reduction of the Ca2+ influx rate via the reverse mode Na+/Ca2+ exchanger might become the limiting factor in digoxin response generation.

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12

Schneider, Jean-Christophe, Driss El Kebir, Christiane Chéreau, Jean-Christophe Mercier, Josette Dall'Ava-Santucci, and A. Tuan Dinh-Xuan. "Involvement of Na+/Ca2+ exchanger in endothelial NO production and endothelium-dependent relaxation." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 2 (August 1, 2002): H837—H844. http://dx.doi.org/10.1152/ajpheart.00789.2001.

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Endothelial nitric oxide (NO) synthase (eNOS) is controlled by Ca2+/calmodulin and caveolin-1 in caveolae. It has been recently suggested that Na+/Ca2+ exchanger (NCX), also expressed in endothelial caveolae, is involved in eNOS activation. To investigate the role played by NCX in NO synthesis, we assessed the effects of Na+ loading (induced by monensin) on rat aortic rings and cultured porcine aortic endothelial cells. Effect of monensin was evaluated by endothelium-dependent relaxation of rat aortic rings in response to acetylcholine and by real-time measurement of NO release from cultured endothelial cells stimulated by A-23187 and bradykinin. Na+ loading shifted the acetylcholine concentration-response curve to the left. These effects were prevented by pretreatment with the NCX inhibitors benzamil and KB-R7943. Monensin potentiated Ca2+-dependent NO release in cultured cells, whereas benzamil and KB-R7943 totally blocked Na+loading-induced NO release. These findings confirm the key role of NCX in reverse mode on Ca2+-dependent NO production and endothelium-dependent relaxation.

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13

Wickley, Peter J., Toshiya Shiga, Paul A. Murray, and Derek S. Damron. "Propofol Modulates Na+–Ca2+Exchange Activity via Activation of Protein Kinase C in Diabetic Cardiomyocytes." Anesthesiology 106, no. 2 (February 1, 2007): 302–11. http://dx.doi.org/10.1097/00000542-200702000-00019.

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Background The authors' objective was to identify the role of the Na+-Ca2+ exchanger (NCX) in mediating the contractile dysfunction observed in diabetic cardiomyocytes before and after exposure to propofol. Methods Freshly isolated ventricular myocytes were obtained from normal and diabetic rat hearts. Intracellular concentration of Ca2+ and cell shortening were simultaneously measured in electrically stimulated, ventricular myocytes using fura-2 and video-edge detection, respectively. Postrest potentiation (PRP) and sarcoplasmic reticulum Ca2+ load were used to assess propofol-induced changes in the activity of the NCX. Results Propofol (10 microM) increased PRP in diabetic cardiomyocytes but had no effect on PRP in normal cardiomyocytes. Removal of sodium enhanced and KB-R7943 (reverse mode NCX inhibitor) blocked PRP in both normal and diabetic cardiomyocytes. In the absence of sodium, propofol enhanced PRP in diabetic cardiomyocytes but had no additional effect in normal cardiomyocytes. KB-R7943 completely blocked propofol-induced potentiation of peak intracellular concentration of Ca2+ and shortening in both cell types. Propofol increased sarcoplasmic reticulum Ca2+ load and prolonged removal of cytosolic Ca2+ in diabetic cardiomyocytes, but not in normal cardiomyocytes. Removal of sodium enhanced propofol-induced increases in sarcoplasmic reticulum Ca2+ load and further prolonged removal of cytosolic Ca2+, whereas KB-R7943 completely blocked propofol-induced increase in sarcoplasmic reticulum Ca2+ load. Protein kinase C inhibition with bisindolylmaleimide I prevented the propofol-induced increase in PRP and prolongation in Ca2+ removal. Conclusions These data suggest that propofol enhances PRP via activation of reverse mode NCX, but attenuates Ca2+ removal from the cytosol via inhibition of forward mode NCX in diabetic cardiomyocytes. The actions of propofol are mediated via a protein kinase C-dependent pathway.

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14

Consolini, A. E., M. I. Ragone, and P. Bonazzola. "Mitochondrial and cytosolic calcium in rat hearts under high-K+ cardioplegia and pyruvate: mechano-energetic performance." Canadian Journal of Physiology and Pharmacology 89, no. 7 (July 2011): 485–96. http://dx.doi.org/10.1139/y11-042.

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High-K+-cardioplegia (CPG) and pyruvate (Pyr) are used as cardioprotective agents. Considering that mitochondria play a critical role in cardiac dysfunction, we investigated the effect of CPG on mitochondrial Ca2+ uptake and sarcorreticular (SR) calcium handling. Cytosolic and mitochondrial Ca2+, as well as mitochondrial membrane potential (ΔΨm) were assessed in rat cardiomyocytes by confocal microscopy. Mechano-calorimetrical correlation was studied in perfused hearts. CPG did not modify JC-1 (ΔΨm), but transiently increased, by up to 1.8 times, the Fura-2 (intracellular Ca concentration, [Ca2+]i) and Rhod-2 (mitochondrial free Ca concentration [Ca2+]m) fluorescence of resting cells, with exponential decays. The addition of 5 µmol·L–1 thapsigargin (Tpg) increased the Rhod-2 fluorescence in a group of cells without any effect on the Fura-2 signal. In rat hearts perfused with CPG, 1 µmol·L–1 Tpg decreased resting heat rate (ΔHr: –0.44 ± 0.07 mW·g–1), while the addition of 5 µmol·L–1 KB-R7943 increased resting pressure (ΔrLVP by +5.26 ± 1.10 mm Hg; 1 mm Hg = 133.322 Pa). The addition of 10 mmol·L–1 Pyr to CPG increased Hr (+3.30 ± 0.24 mW·g–1) and ΔrLVP (+2.2 ± 0.4 mm Hg), which are effects potentiated by KB-R7943. The results suggest that under CPG, (i) there was an increase in [Ca2+]i and [Ca2+]m (without changing ΔΨm) that decayed by exothermic removal mechanisms; (ii) mitochondrial Ca2+ uptake contributed to the removal of cytosolic Ca2+, in a process that was potentiated by inhibition of sarco–endoplasmic reticulum Ca2+-ATPase (SERCA), and reduced by KB-R7943; (iii) under these conditions, SERCA represents the main energetic consumer; (iv) Pyr increased the energetic performance of hearts,mainly by inducing mitochondrial metabolism.

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15

Xu, Lin, Christiana S. Kappler, Santhosh K. Mani, Neal R. Shepherd, Ludivine Renaud, Paige Snider, Simon J. Conway, and Donald R. Menick. "Chronic Administration of KB-R7943 Induces Up-regulation of Cardiac NCX1." Journal of Biological Chemistry 284, no. 40 (August 6, 2009): 27265–72. http://dx.doi.org/10.1074/jbc.m109.022855.

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16

ISAAC, MICHAEL R., CHADWICK L. ELIAS, HOA D. LE, ALEXANDER OMELCHENKO, MARK HNATOWICH, and LARRY V. HRYSHKO. "Inhibition of the Drosophila Na+/Ca2+ Exchanger, CALX1.1, by KB-R7943." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 543–45. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04791.x.

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17

Abramochkin, Denis V., Eugenia I. Alekseeva, and Matti Vornanen. "Inhibition of the cardiac inward rectifier potassium currents by KB-R7943." Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 158, no. 3 (September 2013): 181–86. http://dx.doi.org/10.1016/j.cbpc.2013.08.001.

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18

Tashiro, Michiko, Hana Inoue, and Masato Konishi. "KB-R7943 inhibits Na+-dependent Mg2+ efflux in rat ventricular myocytes." Journal of Physiological Sciences 60, no. 6 (September 23, 2010): 415–24. http://dx.doi.org/10.1007/s12576-010-0113-z.

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19

Abramochkin, Denis V., and Matti Vornanen. "Inhibition of the cardiac ATP-dependent potassium current by KB-R7943." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 175 (September 2014): 38–45. http://dx.doi.org/10.1016/j.cbpa.2014.05.005.

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20

Kraft, Robert. "The Na+/Ca2+ exchange inhibitor KB-R7943 potently blocks TRPC channels." Biochemical and Biophysical Research Communications 361, no. 1 (September 2007): 230–36. http://dx.doi.org/10.1016/j.bbrc.2007.07.019.

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21

Zhang, Shen, Jason X. J. Yuan, Kim E. Barrett, and Hui Dong. "Role of Na+/Ca2+ exchange in regulating cytosolic Ca2+ in cultured human pulmonary artery smooth muscle cells." American Journal of Physiology-Cell Physiology 288, no. 2 (February 2005): C245—C252. http://dx.doi.org/10.1152/ajpcell.00411.2004.

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A rise in cytosolic Ca2+ concentration ([Ca2+]cyt) in pulmonary artery smooth muscle cells (PASMC) is an important stimulus for cell contraction, migration, and proliferation. Depletion of intracellular Ca2+ stores opens store-operated Ca2+ channels (SOC) and causes Ca2+ entry. Transient receptor potential (TRP) cation channels that are permeable to Na+ and Ca2+ are believed to form functional SOC. Because sarcolemmal Na+/Ca2+ exchanger has also been implicated in regulating [Ca2+]cyt, this study was designed to test the hypothesis that the Na+/Ca2+ exchanger (NCX) in cultured human PASMC is functionally involved in regulating [Ca2+]cyt by contributing to store depletion-mediated Ca2+ entry. RT-PCR and Western blot analyses revealed mRNA and protein expression for NCX1 and NCKX3 in cultured human PASMC. Removal of extracellular Na+, which switches the Na+/Ca2+ exchanger from the forward (Ca2+ exit) to reverse (Ca2+ entry) mode, significantly increased [Ca2+]cyt, whereas inhibition of the Na+/Ca2+ exchanger with KB-R7943 (10 μM) markedly attenuated the increase in [Ca2+]cyt via the reverse mode of Na+/Ca2+ exchange. Store depletion also induced a rise in [Ca2+]cyt via the reverse mode of Na+/Ca2+ exchange. Removal of extracellular Na+ or inhibition of the Na+/Ca2+ exchanger with KB-R7943 attenuated the store depletion-mediated Ca2+ entry. Furthermore, treatment of human PASMC with KB-R7943 also inhibited cell proliferation in the presence of serum and growth factors. These results suggest that NCX is functionally expressed in cultured human PASMC, that Ca2+ entry via the reverse mode of Na+/Ca2+ exchange contributes to store depletion-mediated increase in [Ca2+]cyt, and that blockade of the Na+/Ca2+ exchanger in its reverse mode may serve as a potential therapeutic approach for treatment of pulmonary hypertension.

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Liskova, Veronika, Sona Hudecova, Lubomira Lencesova, Filippo Iuliano, Marta Sirova, Karol Ondrias, Silvia Pastorekova, and Olga Krizanova. "Type 1 Sodium Calcium Exchanger Forms a Complex with Carbonic Anhydrase IX and Via Reverse Mode Activity Contributes to pH Control in Hypoxic Tumors." Cancers 11, no. 8 (August 9, 2019): 1139. http://dx.doi.org/10.3390/cancers11081139.

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Hypoxia and acidosis are among the key microenvironmental factors that contribute to cancer progression. We have explored a possibility that the type 1Na+/Ca2+ exchanger (NCX1) is involved in pH control in hypoxic tumors. We focused on changes in intracellular pH, co-localization of NCX1, carbonic anhydrase IX (CA IX), and sodium proton exchanger type 1 (NHE1) by proximity ligation assay, immunoprecipitation, spheroid formation assay and migration of cells due to treatment with KB-R7943, a selective inhibitor of the reverse-mode NCX1. In cancer cells exposed to hypoxia, reverse-mode NCX1 forms a membrane complex primarily with CA IX and also with NHE1. NCX1/CA IX/NHE1 assembly operates as a metabolon with a potent ability to extrude protons to the extracellular space and thereby facilitate acidosis. KB-R7943 prevents formation of this metabolon and reduces cell migration. Thus, we have shown that in hypoxic cancer cells, NCX1 operates in a reverse mode and participates in pH regulation in hypoxic tumors via cooperation with CAIX and NHE1.

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Newton, Jamila, Luli Rebecca Akinfiresoye, and Prosper N’Gouemo. "Inhibition of the Sodium Calcium Exchanger Suppresses Alcohol Withdrawal-Induced Seizure Susceptibility." Brain Sciences 11, no. 2 (February 23, 2021): 279. http://dx.doi.org/10.3390/brainsci11020279.

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Calcium influx plays important roles in the pathophysiology of seizures, including acoustically evoked alcohol withdrawal-induced seizures (AWSs). One Ca2+ influx route of interest is the Na+/Ca2+ exchanger (NCX) that, when operating in its reverse mode (NCXrev) activity, can facilitate Ca2+ entry into neurons, possibly increasing neuronal excitability that leads to enhanced seizure susceptibility. Here, we probed the involvement of NCXrev activity on AWS susceptibility by quantifying the effects of SN-6 and KB-R7943, potent blockers of isoform type 1 (NCX1rev) and 3 (NCX3rev), respectively. Male, adult Sprague–Dawley rats were used. Acoustically evoked AWSs consisted of wild running seizures (WRSs) that evolved into generalized tonic–clonic seizures (GTCSs). Quantification shows that acute SN-6 treatment at a relatively low dose suppressed the occurrence of the GTCSs (but not WRSs) component of AWSs and markedly reduced the seizure severity. However, administration of KB-R7943 at a relatively high dose only reduced the incidence of GTCSs. These findings demonstrate that inhibition of NCX1rev activity is a putative mechanism for the suppression of alcohol withdrawal-induced GTCSs.

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Yang, Dingwei, Dingping Yang, Ruhan Jia, and Jin Tan. "Na+/Ca2+ exchange inhibitor, KB-R7943, attenuates contrast-induced acute kidney injury." Journal of Nephrology 26, no. 5 (2013): 877–85. http://dx.doi.org/10.5301/jn.5000259.

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Hashimoto, Keltaro, Shigeki Miyamoto, Bing-Mel Zhu, and Kazunori Kamiya. "A exchange inhibitor, KB-R7943, on digitalis and ischemia-reperfusion arrhythmia models." Journal of Molecular and Cellular Cardiology 33, no. 6 (June 2001): A45. http://dx.doi.org/10.1016/s0022-2828(01)90176-2.

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Arakawa, Naohisa, Masaki Sakaue, Ikuko Yokoyama, Hitoshi Hashimoto, Yutaka Koyama, Akemichi Baba, and Toshio Matsuda. "KB-R7943 Inhibits Store-Operated Ca2+ Entry in Cultured Neurons and Astrocytes." Biochemical and Biophysical Research Communications 279, no. 2 (December 2000): 354–57. http://dx.doi.org/10.1006/bbrc.2000.3968.

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Yamamura, K. "Very low dose of the Na+/Ca2+ exchange inhibitor, KB-R7943, protects ischemic reperfused aged Fischer 344 rat hearts: considerable strain difference in the sensitivity to KB-R7943." Cardiovascular Research 52, no. 3 (December 2001): 397–406. http://dx.doi.org/10.1016/s0008-6363(01)00409-6.

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Ladilov, Y., S. Haffner, C. Balser-Schäfer, H. Maxeiner, and H. M. Piper. "Cardioprotective effects of KB-R7943: a novel inhibitor of the reverse mode of Na+/Ca2+exchanger." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1868—H1876. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1868.

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The novel inhibitor of the reverse mode of the Na+/Ca2+exchanger (NCE) KB-R7943 (KB) was tested in isolated rat cardiomyocytes exposed to 80 min of simulated ischemia [substrate-free anoxia, extracellular pH (pHo) of 6.4] and 15 min of reoxygenation (pHo 7.4). At pHo 6.4, 20 μmol/l KB was required for complete inhibition of the reverse mode of NCE. Treatment with 20 μmol/l KB only during anoxia did not influence the onset of rigor contracture and intracellular pH (pHi) (monitored with 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein) but significantly reduced the cytosolic accumulation of Ca2+ (monitored with fura 2) and Na+ (monitored with sodium-binding benzofuran isophthalate). During reoxygenation, cardiomyocytes developed hypercontracture. This was significantly reduced by anoxic KB treatment. To investigate this protection against reoxygenation-induced injury in the whole heart, we exposed Langendorff-perfused rat hearts to 110 min of anoxia (pHo 6.4) and 50 min of reoxygenation (pHo 7.4). Application of 20 μmol/l KB during anoxia significantly reduced the reoxygenation-induced enzyme release. We conclude that KB offers significant protection of cardiomyocytes against Ca2+ and Na+ overload during anoxia and hypercontracture or enzyme release on reoxygenation.

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Islam, MS, T. Akhter, and M. Matsumoto. "Asterosap, an Egg Jelly Peptide, Elevate Intracellular Ca²⁺ and Activate the Motility of Spermatozoa." Progressive Agriculture 19, no. 1 (December 18, 2013): 79–88. http://dx.doi.org/10.3329/pa.v19i1.17358.

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Components from the outer envelopes of the egg that influence the flagellar beating and acrosome reaction of spermatozoa are regulated by ion flux across the plasma membrane. Asterosap, a sperm-activating peptide from the starfish egg jelly layer, causes a transient increase in intracellular cyclic GMP (cGMP) through the activation of the asterosap receptor, a guanylyl cyclase (GC), and causes an increase in intracellular Ca2+. Here we describe the pathway of asterosap-induced Ca2+ elevation using different Ca2+ channel antagonists. Fluo-4 AM, a cell permeable Ca2+ sensitive dye was used to determine the channel caused by the asterosap-induced Ca2+ elevation in spermatozoa. Different L-type Ca2+ channel antagonists, a non specific Ca2+ channel antagonist (nickel chloride), and a store-operated Ca2+ channel (SOC) antagonist do not show any significant response on asterosap-induced Ca2+ elevation, whereas KB-R7943, a selective inhibitor against Na+/Ca2+ exchanger (NCX) inhibited effectively. We also analyzed the flagellar movement of spermatozoa in artificial seawater (ASW) containing the asterosap at 100 nM ml?1. We found that spermatozoa swam vigorously with more symmetrical flagellar movement in asterosap than in ASW and KB-R7943 significantly inhibited the flagellar movement.DOI: http://dx.doi.org/10.3329/pa.v19i1.17358 Progress. Agric. 19(1): 79 - 88, 2008

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Tedesco, Scattolini, Albiero, Bortolozzi, Avogaro, Cignarella, and Fadini. "Mitochondrial Calcium Uptake Is Instrumental to Alternative Macrophage Polarization and Phagocytic Activity." International Journal of Molecular Sciences 20, no. 19 (October 8, 2019): 4966. http://dx.doi.org/10.3390/ijms20194966.

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Macrophages are highly plastic and dynamic cells that exert much of their function through phagocytosis. Phagocytosis depends on a coordinated, finely tuned, and compartmentalized regulation of calcium concentrations. We examined the role of mitochondrial calcium uptake and mitochondrial calcium uniporter (MCU) in macrophage polarization and function. In primary cultures of human monocyte-derived macrophages, calcium uptake in mitochondria was instrumental for alternative (M2) macrophage polarization. Mitochondrial calcium uniporter inhibition with KB-R7943 or MCU knockdown, which prevented mitochondrial calcium uptake, reduced M2 polarization, while not affecting classical (M1) polarization. Challenging macrophages with E. coli fragments induced spikes of mitochondrial calcium concentrations, which were prevented by MCU inhibition or silencing. In addition, mitochondria remodelled in M2 macrophages during phagocytosis, especially close to sites of E. coli internalization. Remarkably, inhibition or knockdown of MCU significantly reduced the phagocytic capacity of M2 macrophages. KB-R7943, which also inhibits the membrane sodium/calcium exchanger and Complex I, reduced mitochondria energization and cellular ATP levels, but such effects were not observed with MCU silencing. Therefore, phagocytosis inhibition by MCU knockdown depended on the impaired mitochondrial calcium buffering rather than changes in mitochondrial and cellular energy status. These data uncover a new role for MCU in alternative macrophage polarization and phagocytic activity.

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Ren, Yongkui, Yunfei Cai, and Dalin Jia. "Comparative Antiapoptotic Effects of KB-R7943 and Ischemic Postconditioning During Myocardial Ischemia Reperfusion." Cell Biochemistry and Biophysics 64, no. 2 (June 17, 2012): 137–45. http://dx.doi.org/10.1007/s12013-012-9382-x.

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Bonazzola, P., P. Egido, F. D. Marengo, E. Savio-Galimberti, and J. E. Ponce-Hornos. "Lithium and KB-R7943 effects on mechanics and energetics of rat heart muscle." Acta Physiologica Scandinavica 176, no. 1 (August 23, 2002): 1–11. http://dx.doi.org/10.1046/j.1365-201x.2002.01001.x.

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Miyata, Akira, Douglas P. Zipes, Stephen Hall, and Michael Rubart. "KB-R7943 Prevents Acute, Atrial Fibrillation–Induced Shortening of Atrial Refractoriness in Anesthetized Dogs." Circulation 106, no. 11 (September 10, 2002): 1410–19. http://dx.doi.org/10.1161/01.cir.0000028587.85711.f6.

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Li, Jia, Hong-Bo Jin, Yan-Ming Sun, Ying Su, and Lan-Feng Wang. "KB-R7943 inhibits high glucose-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion." Biochemical and Biophysical Research Communications 392, no. 4 (February 2010): 516–19. http://dx.doi.org/10.1016/j.bbrc.2009.12.183.

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Chang, Po-Cheng, Hung-Ta Wo, Hui-Ling Lee, Ming-Shien Wen, and Chung-Chuan Chou. "Paradoxical effects of KB-R7943 on arrhythmogenicity in a chronic myocardial infarction rabbit model." Journal of Cardiology 66, no. 1 (July 2015): 80–87. http://dx.doi.org/10.1016/j.jjcc.2014.08.002.

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Storozhevykh, T. P., Ya E. Senilova, T. Brustovetsky, V. G. Pinelis, and N. Brustovetsky. "Neuroprotective Effect of KB-R7943 Against Glutamate Excitotoxicity is Related to Mild Mitochondrial Depolarization." Neurochemical Research 35, no. 2 (September 22, 2009): 323–35. http://dx.doi.org/10.1007/s11064-009-0058-x.

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Peralta-Arias, Rubén D., Carmen Y. Vívenes, María I. Camejo, Sandy Piñero, Teresa Proverbio, Elizabeth Martínez, Reinaldo Marín, and Fulgencio Proverbio. "ATPases, ion exchangers and human sperm motility." REPRODUCTION 149, no. 5 (May 2015): 475–84. http://dx.doi.org/10.1530/rep-14-0471.

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Human sperm has several mechanisms to control its ionic milieu, such as the Na,K-ATPase (NKA), the Ca-ATPase of the plasma membrane (PMCA), the Na+/Ca2+-exchanger (NCX) and the Na+/H+-exchanger (NHE). On the other hand, the dynein-ATPase is the intracellular motor for sperm motility. In this work, we evaluated NKA, PMCA, NHE, NCX and dynein-ATPase activities in human sperm and investigated their correlation with sperm motility. Sperm motility was measured by Computer Assisted Semen Analysis. It was found that the NKA activity is inhibited by ouabain with twoKi(7.9×10−9and 9.8×10−5 M), which is consistent with the presence of two isoforms of α subunit of the NKA in the sperm plasma membranes (α1 and α4), being α4 more sensitive to ouabain. The decrease in NKA activity is associated with a reduction in sperm motility. In addition, sperm motility was evaluated in the presence of known inhibitors of NHE, PMCA and NCX, such as amiloride, eosin, and KB-R7943, respectively, as well as in the presence of nigericin after incubation with ouabain. Amiloride, eosin and KB-R7943 significantly reduced sperm motility. Nigericin reversed the effect of ouabain and amiloride on sperm motility. Dynein-ATPase activity was inhibited by acidic pH and micromolar concentrations of Ca2+. We explain our results in terms of inhibition of the dynein-ATPase in the presence of higher cytosolic H+and Ca2+, and therefore inhibition of sperm motility.

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Yoshitomi, Osamu, Tetsuya Hara, Sungsam Cho, Shiro Tomiyasu, and Koji Sumikawa. "Cardioprotective Effects of KB-R7943, a Na+/Ca2+ Exchanger Inhibitor, on Stunned Myocardium in Dogs." Anesthesiology 96, Sup 2 (September 2002): A600. http://dx.doi.org/10.1097/00000542-200209002-00600.

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Hojo, Minoru, Takeshi Ono, Hiroyuki Yamada, Shirou Tomiyasu, and Koji Sumikawa. "The Effect of Na+/Ca2+ Exchanger Inhibitor, KB-R7943, on the Formalin Test in Mice." Anesthesiology 96, Sup 2 (September 2002): A843. http://dx.doi.org/10.1097/00000542-200209002-00843.

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Stains, Joseph P., and Carol V. Gay. "Inhibition of Na+/Ca2+ Exchange with KB-R7943 or Bepridil Diminishes Mineral Deposition by Osteoblasts." Journal of Bone and Mineral Research 16, no. 8 (August 1, 2001): 1434–43. http://dx.doi.org/10.1359/jbmr.2001.16.8.1434.

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NAKAMURA, Aki, Kengo HARADA, Hisako SUGIMOTO, Fumio NAKAJIMA, and Noriyasu NISHIMURA. "Effects of KB-R7943, a novel Na+/Ca2+ exchange inhibitor, on myocardial ischemia/reperfusion injury." Folia Pharmacologica Japonica 111, no. 2 (1998): 105–15. http://dx.doi.org/10.1254/fpj.111.105.

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Iwamoto, Takahiro, Satomi Kita, Akira Uehara, Yutaka Inoue, Yuki Taniguchi, Issei Imanaga, and Munekazu Shigekawa. "Structural Domains Influencing Sensitivity to Isothiourea Derivative Inhibitor KB-R7943 in Cardiac Na+/Ca2+Exchanger." Molecular Pharmacology 59, no. 3 (March 1, 2001): 524–31. http://dx.doi.org/10.1124/mol.59.3.524.

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Lu, Jing, Yong Liang, and Xiaoliang Wang. "Amiloride and KB-R7943 in Outward Na+/Ca2+ Exchange Current in Guinea Pig Ventricular Myocytes." Journal of Cardiovascular Pharmacology 40, no. 1 (July 2002): 106–11. http://dx.doi.org/10.1097/00005344-200207000-00013.

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Cheng, Hongwei, Yihong Zhang, Chunyun Du, Christopher E. Dempsey, and Jules C. Hancox. "High potency inhibition of hERG potassium channels by the sodium-calcium exchange inhibitor KB-R7943." British Journal of Pharmacology 165, no. 7 (March 9, 2012): 2260–73. http://dx.doi.org/10.1111/j.1476-5381.2011.01688.x.

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Watano, Tomokazu, Yoshimitsu Harada, Kengo Harada, and Noriyasu Nishimura. "Effect of Na+ /Ca2+ exchange inhibitor, KB-R7943 on ouabain-induced arrhythmias in guinea-pigs." British Journal of Pharmacology 127, no. 8 (August 1999): 1846–50. http://dx.doi.org/10.1038/sj.bjp.0702740.

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LI, LIBING, and JUNKO KIMURA. "Effect of KB-R7943 on Oscillatory Na+/Ca2+ Exchange Current in Guinea Pig Ventricular Myocytes." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 539–42. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04790.x.

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Su, Ying, Nan Mao, Min Li, Xia Dong, Fan-Zhen Lin, Ying Xu, and Yan-Bo Li. "KB-R7943 restores endothelium-dependent relaxation induced by advanced glycosylation end products in rat aorta." Journal of Diabetes and its Complications 27, no. 1 (January 2013): 6–10. http://dx.doi.org/10.1016/j.jdiacomp.2012.08.007.

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Hirota, Simon, Evi Pertens, and Luke J. Janssen. "The reverse mode of the Na+/Ca2+ exchanger provides a source of Ca2+ for store refilling following agonist-induced Ca2+ mobilization." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (February 2007): L438—L447. http://dx.doi.org/10.1152/ajplung.00222.2006.

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Agonist-induced contraction of airway smooth muscle (ASM) can be triggered by an elevation in the intracellular Ca2+ concentration, primarily through the release of Ca2+ from the sarcoplasmic reticulum (SR). The refilling of the SR is integral for subsequent contractions. It has been suggested that Ca2+ entry via store-operated cation (SOC) and receptor-operated cation channels may facilitate refilling of the SR. Indeed, depletion of the SR activates substantial inward SOC currents in ASM that are composed of both Ca2+ and Na+. Accumulation of Na+ within the cell may regulate Ca2+ handling in ASM by forcing the Na+/Ca2+ exchanger (NCX) into the reverse mode, leading to the influx of Ca2+ from the extracellular domain. Since depletion of the SR activates substantial inward Na+ current, it is conceivable that the reverse mode of the NCX may contribute to the intracellular Ca2+ pool from which the SR is refilled. Indeed, successive contractions of bovine ASM, evoked by various agonists (ACh, histamine, 5-HT, caffeine) were significantly reduced upon removal of extracellular Na+; whereas contractions evoked by KCl were unchanged by Na+ depletion. Ouabain, a selective inhibitor of the Na+/K+ pump, had no effect on the reductions observed under normal and zero-Na+ conditions. KB-R7943, a selective inhibitor of the reverse mode of the NCX, significantly reduced successive contractions induced by all agonists without altering KCl responses. Furthermore, KB-R7943 abolished successive caffeine-induced Ca2+ transients in single ASM cells. Together, these data suggest a role for the reverse mode of the NCX in refilling the SR in ASM following Ca2+ mobilization.

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de Ruijter, Wouter, Ger J. M. Stienen, Jan van Klarenbosch, and Jacob J. de Lange. "Negative and Positive Inotropic Effects of Propofol via L-type Calcium Channels and the Sodium-Calcium Exchanger in Rat Cardiac Trabeculae." Anesthesiology 97, no. 5 (November 1, 2002): 1146–55. http://dx.doi.org/10.1097/00000542-200211000-00019.

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Background Conflicting opinions are present in the literature regarding the origin of the negative inotropic effect of propofol on the myocardium. This study aims to resolve these discrepancies by investigating the inotropic effects of propofol the L-type calcium channels and the sodium-calcium exchanger (NCX). Methods The effect of 20 microg/ml propofol on force development was determined in rat cardiac trabeculae at different pacing frequencies and different extracellular calcium concentrations. Postrest potentiation, sodium withdrawal during quiescence, and the NCX inhibitor KB-R7943 were used to study changes in the activity of the reverse mode of the NCX by propofol. Results The effect of propofol on steady state peak force depended on pacing frequency and calcium concentration. A negative inotropic effect was observed at pacing frequencies greater than 0.5 Hz, but a positive inotropic effect was observed at 0.1 Hz and low calcium, which cannot be explained by an effect on the L-type calcium channel. Propofol enhanced postrest potentiation in a calcium-dependent manner. Sodium withdrawal during quiescence and the use of the specific NCX inhibitor KB-R7943 provided evidence for an enhancement of calcium influx by propofol the reverse mode of the NCX. Conclusions The effects of propofol on the myocardium depend on pacing frequency and calcium concentration. The positive inotropic effect of propofol is associated with increased calcium influx the reverse mode of the NCX. The authors conclude that the net inotropic effect of propofol is the result of its counteracting influence on the functioning of the L-type calcium channel and the NCX.

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Dong, Hui, Ki-Nam Shim, Jenny M. J. Li, Christine Estrema, Tiffany A. Ornelas, Flang Nguyen, Shanglei Liu, et al. "Molecular mechanisms underlying Ca2+-mediated motility of human pancreatic duct cells." American Journal of Physiology-Cell Physiology 299, no. 6 (December 2010): C1493—C1503. http://dx.doi.org/10.1152/ajpcell.00242.2010.

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We recently reported that transforming growth factor-β (TGF-β) induces an increase in cytosolic Ca2+ ([Ca2+]cyt) in pancreatic cancer cells, but the mechanisms by which TGF-β mediates [Ca2+]cyt homeostasis in these cells are currently unknown. Transient receptor potential (TRP) channels and Na+/Ca2+ exchangers (NCX) are plasma membrane proteins that play prominent roles in controlling [Ca2+]cyt homeostasis in normal mammalian cells, but little is known regarding their roles in the regulation of [Ca2+]cyt in pancreatic cancer cells and pancreatic cancer development. Expression and function of NCX1 and TRPC1 proteins were characterized in BxPc3 pancreatic cancer cells. TGF-β induced both intracellular Ca2+ release and extracellular Ca2+ entry in these cells; however, 2-aminoethoxydiphenyl borate [2-APB; a blocker for both inositol 1,4,5-trisphosphate (IP3) receptor and TRPC], LaCl3 (a selective TRPC blocker), or KB-R7943 (a selective inhibitor for the Ca2+ entry mode of NCX) markedly inhibited the TGF-β-induced increase in [Ca2+]cyt. 2-APB or KB-R7943 treatment was able to dose-dependently reverse membrane translocation of PKCα induced by TGF-β. Transfection with small interfering RNA (siRNA) against NCX1 almost completely abolished NCX1 expression in BxPc3 cells and also inhibited PKCα serine phosphorylation induced by TGF-β. Knockdown of NCX1 or TRPC1 by specific siRNA transfection reversed TGF-β-induced pancreatic cancer cell motility. Therefore, TGF-β induces Ca2+ entry likely via TRPC1 and NCX1 and raises [Ca2+]cyt in pancreatic cancer cells, which is essential for PKCα activation and subsequent tumor cell invasion. Our data suggest that TRPC1 and NCX1 may be among the potential therapeutic targets for pancreatic cancer.

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