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Journal articles on the topic 'SEA0400'

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Author: Grafiati

Published: 4 June 2021

Last updated: 6 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

Zhang, Jin, Chongyu Ren, Ling Chen, Manuel F. Navedo, Laura K. Antos, Stephen P. Kinsey, Takahiro Iwamoto, et al. "Knockout of Na+/Ca2+ exchanger in smooth muscle attenuates vasoconstriction and L-type Ca2+ channel current and lowers blood pressure." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 5 (May 2010): H1472—H1483. http://dx.doi.org/10.1152/ajpheart.00964.2009.

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Mice with smooth muscle (SM)-specific knockout of Na+/Ca2+ exchanger type-1 (NCX1SM−/−) and the NCX inhibitor, SEA0400, were used to study the physiological role of NCX1 in mouse mesenteric arteries. NCX1 protein expression was greatly reduced in arteries from NCX1SM−/− mice generated with Cre recombinase. Mean blood pressure (BP) was 6–10 mmHg lower in NCX1SM−/− mice than in wild-type (WT) controls. Vasoconstriction was studied in isolated, pressurized mesenteric small arteries from WT and NCX1SM−/− mice and in heterozygotes with a global null mutation (NCX1Fx/−). Reduced NCX1 activity was manifested by a marked attenuation of responses to low extracellular Na+ concentration, nanomolar ouabain, and SEA0400. Myogenic tone (MT, 70 mmHg) was reduced by ∼15% in NCX1SM−/− arteries and, to a similar extent, by SEA0400 in WT arteries. MT was normal in arteries from NCX1Fx/− mice, which had normal BP. Vasoconstrictions to phenylephrine and elevated extracellular K+ concentration were significantly reduced in NCX1SM−/− arteries. Because a high extracellular K+ concentration-induced vasoconstriction involves the activation of L-type voltage-gated Ca2+ channels (LVGCs), we measured LVGC-mediated currents and Ca2+ sparklets in isolated mesenteric artery myocytes. Both the currents and the sparklets were significantly reduced in NCX1SM−/− (vs. WT or NCX1Fx/−) myocytes, but the voltage-dependent inactivation of LVGCs was not augmented. An acute application of SEA0400 in WT myocytes had no effect on LVGC current. The LVGC agonist, Bay K 8644, eliminated the differences in LVGC currents and Ca2+ sparklets between NCX1SM−/− and control myocytes, suggesting that LVGC expression was normal in NCX1SM−/− myocytes. Bay K 8644 did not, however, eliminate the difference in myogenic constriction between WT and NCX1SM−/− arteries. We conclude that, under physiological conditions, NCX1-mediated Ca2+ entry contributes significantly to the maintenance of MT. In NCX1SM−/− mouse artery myocytes, the reduced Ca2+ entry via NCX1 may lower cytosolic Ca2+ concentration and thereby reduce MT and BP. The reduced LVGC activity may be the consequence of a low cytosolic Ca2+ concentration.

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3

Tanaka, Yusuke, Kae Obata, Tamano Ohmori, Kohei Ishiwata, Manato Abe, Shogo Hamaguchi, Iyuki Namekata, and Hikaru Tanaka. "Angiotensin II Induces Automatic Activity of the Isolated Guinea Pig Pulmonary Vein Myocardium through Activation of the IP3 Receptor and the Na+-Ca2+ Exchanger." International Journal of Molecular Sciences 20, no. 7 (April 10, 2019): 1768. http://dx.doi.org/10.3390/ijms20071768.

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The automaticity of the pulmonary vein myocardium is known to be the major cause of atrial fibrillation. We examined the involvement of angiotensin II in the automatic activity of isolated guinea pig pulmonary vein preparations. In tissue preparations, application of angiotensin II induced an automatic contractile activity; this effect was mimicked by angiotensin I and blocked by losartan, but not by PD123,319 or carvedilol. In cardiomyocytes, application of angiotensin II induced an increase in the frequency of spontaneous Ca2+ sparks and the generation of Ca2+ transients; these effects were inhibited by losartan or xestospongin C. In tissue preparations, angiotensin II caused membrane potential oscillations, which lead to repetitive generation of action potentials. Angiotensin II increased the diastolic depolarization slope of the spontaneous or evoked action potentials. These effects of angiotensin II were inhibited by SEA0400. In tissue preparations showing spontaneous firing of action potentials, losartan, xestospongin C or SEA0400 decreased the slope of the diastolic depolarization and inhibited the firing of action potentials. In conclusion, in the guinea pig pulmonary vein myocardium, angiotensin II induces the generation of automatic activity through activation of the IP3 receptor and the Na+-Ca2+ exchanger.

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4

Amran, M. S., N. Homma, and K. Hashimoto. "Effects of SEA0400 on Ouabain-induced Arrhythmias in Guinea Pigs." Journal of Scientific Research 4, no. 1 (December 26, 2011): 213. http://dx.doi.org/10.3329/jsr.v4i1.7722.

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The sodium-calcium exchange (NCX) is one of the major regulators of intracellular Ca2+ concentration in cardiac myocytes. The effects of NCX blockers as antiarrhythmic agents are still controversial. We investigated antiarrhythmic effects of SEA0400 (SEA), a novel NCX inhibitor, on ouabain-induced arrhythmias in guinea pigs. In the whole animal arrhythmia model, we observed effects of SEA on the ouabain-induced arrhythmia using ECG recordings. In the isolated myocyte, we observed action potential configurations and oscillations due to calcium overload using the current clamp method. In the whole animal model, SEA at a dose range of 1-10 mg/kg (intravenous, bolus) suppressed ouabain-induced arrhythmias dose-dependently. In isolated ventricular myocytes, SEA (0.1-3 µM) suppressed ouabain-induced oscillatory activity observed between action potentials. SEA (0.1-3 µM) also suppressed ouabain-induced NCX current (INCX) that is also called transient inward current (ITI). Our results indicate that NCX is involved in arrhythmia and oscillatory activity induced by ouabain. The inhibition of these arrhythmias and oscillatory activity by SEA might result from the inhibition of NCX.Keywords: Na+-Ca2+ exchange (NCX); SEA0400; NCX inhibitors; current clamp; ECG.© 2012 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved.doi: http://dx.doi.org/10.3329/jsr.v4i1.7722J. Sci. Res. 4 (1), 213-225 (2012)

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5

Lee, Candace, and Larry V. Hryshko. "SEA0400: A Novel Sodium-Calcium Exchange Inhibitor with Cardioprotective Properties1." Cardiovascular Drug Reviews 22, no. 4 (June 7, 2006): 334–47. http://dx.doi.org/10.1111/j.1527-3466.2004.tb00150.x.

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6

Iwamoto, Takahiro, Satomi Kita, Akira Uehara, Issei Imanaga, Toshio Matsuda, Akemichi Baba, and Takeshi Katsuragi. "Molecular Determinants of Na+/Ca2+Exchange (NCX1) Inhibition by SEA0400." Journal of Biological Chemistry 279, no. 9 (December 5, 2003): 7544–53. http://dx.doi.org/10.1074/jbc.m310491200.

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7

Iwamoto, Takahiro. "Vascular Na+/Ca2+ exchanger: implications for the pathogenesis and therapy of salt-dependent hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 3 (March 2006): R536—R545. http://dx.doi.org/10.1152/ajpregu.00592.2005.

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The Na+/Ca2+ exchanger is an ion transporter that exchanges Na+ and Ca2+ in either Ca2+ efflux or Ca2+ influx mode, depending on membrane potential and transmembrane ion gradients. In arterial smooth muscle cells, the Na+/Ca2+ exchanger is thought to participate in the maintenance of vascular tone by regulating cytosolic Ca2+ concentration. Recent pharmacological and genetic engineering studies have revealed that the Ca2+ influx mode of vascular Na+/Ca2+ exchanger type-1 (NCX1) is involved in the pathogenesis of salt-dependent hypertension. SEA0400, a specific Na+/Ca2+ exchange inhibitor that preferentially blocks the Ca2+ influx mode, lowers arterial blood pressure in salt-dependent hypertensive models, but not in normotensive rats or other types of hypertensive rats. Furthermore, heterozygous mice with reduced expression of NCX1 are resistant to development of salt-dependent hypertension, whereas transgenic mice with vascular smooth muscle-specific overexpression of NCX1 readily develop hypertension after high-salt loading. SEA0400 reverses the cytosolic Ca2+ elevation and vasoconstriction induced by nanomolar ouabain, as well as humoral factors in salt-loaded animals. One possibility is that circulating endogenous cardiotonic steroids may be necessary for NCX1-mediated hypertension. These findings help to explain how arterial smooth muscle cells in blood vessels contribute to salt-elicited blood pressure elevation and suggest that NCX1 inhibitors might be therapeutically useful for salt-dependent hypertension.

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8

Saesue, Prajak, Tetsuyoshi Horiuchi, Tetsuya Goto, Yuichiro Tanaka, and Kazuhiro Hongo. "Functional role of the Na+/H+ exchanger in the regulation of cerebral arteriolar tone in rats." Journal of Neurosurgery 101, no. 2 (August 2004): 330–35. http://dx.doi.org/10.3171/jns.2004.101.2.0330.

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Object. In vascular smooth-muscle cells, the Na+/H+ exchanger (NHE) is involved in the regulation of [Na+]i, pHi through [H+], and cell volume. Recently, investigations have determined that this exchanger contributes to ischemia and reperfusion injury in coronary circulation. Nonetheless, there is limited information on this glycoprotein in cerebral circulation, especially microcirculation. Thus, the authors in the present study examined the role of NHE in the regulation of cerebral arteriolar tone and its related mechanisms in vitro. Methods. The internal diameter of isolated pressurized intracerebral arterioles in rats was monitored with the aid of a microscope. To examine the basal activity of NHE two kinds of Na+/H+ exchange inhibitors (FR183998 and 5-[N,N-hexamethylene] amiloride) were administered in the arterioles. Furthermore the authors studied the effects of nitric oxide (NO) synthase inhibitor (NG methyl-l-arginine), Na+/K+—adenosine triphosphatase (NKA) inhibitor (ouabain), and the Na+/Ca++ exchange inhibitor (SEA0400) on the vascular response induced by either of the Na+/H+ exchange inhibitors. Both of the Na+/H+ exchange inhibitors constricted the arteriole. Subsequent application of NO synthase inhibitor further decreased the diameter of the arterioles. The Na+/H+ exchange inhibitor—induced constriction was completely abolished in the presence of ouabain and SEA0400. Conclusions. The NHE is active in the basal condition and regulates cerebral arteriolar tone through NKA and the Na+/Ca++ exchanger. Endogenous NO is not related to the activity of NHE in basal conditions.

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9

Namekata, Iyuki, Hideaki Shimada, Toru Kawanishi, Hikaru Tanaka, and Koki Shigenobu. "Reduction by SEA0400 of myocardial ischemia-induced cytoplasmic and mitochondrial Ca2+ overload." European Journal of Pharmacology 543, no. 1-3 (August 2006): 108–15. http://dx.doi.org/10.1016/j.ejphar.2006.06.012.

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10

Bouchard, Ron, Alexander Omelchenko, Hoa Dinh Le, Platon Choptiany, Toshio Matsuda, Akemichi Baba, Kenzo Takahashi, et al. "Effects of SEA0400 on Mutant NCX1.1 Na+-Ca2+ Exchangers with Altered Ionic Regulation." Molecular Pharmacology 65, no. 3 (February 19, 2004): 802–10. http://dx.doi.org/10.1124/mol.65.3.802.

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11

Tanaka, Hikaru, Kazuhide Nishimaru, Tokiko Aikawa, Wataru Hirayama, Yoshio Tanaka, and Koki Shigenobu. "Effect of SEA0400, a novel inhibitor of sodium-calcium exchanger, on myocardial ionic currents." British Journal of Pharmacology 135, no. 5 (March 2002): 1096–100. http://dx.doi.org/10.1038/sj.bjp.0704574.

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12

de la Cruz, Gemma Guedes, Klaus Groschner, C. Oliver Kappe, and Toma N. Glasnov. "High-speed microwave assisted synthesis of SEA0400—a selective inhibitor of the Na+/Ca2+ exchanger." Tetrahedron Letters 53, no. 29 (July 2012): 3731–34. http://dx.doi.org/10.1016/j.tetlet.2012.04.120.

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13

CHOU, CHUNG-CHUAN, PO-CHENG CHANG, MING-SHIEN WEN, HUI-LING LEE, YEN CHU, AKEMICHI BABA, TOSHIO MATSUDA, SAN-JOU YEH, and DELON WU. "Effects of SEA0400 on Arrhythmogenicity in a Langendorff-Perfused 1-Month Myocardial Infarction Rabbit Model." Pacing and Clinical Electrophysiology 36, no. 5 (February 4, 2013): 596–606. http://dx.doi.org/10.1111/pace.12091.

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14

Ogata, Masaya, Takahiro Iwamoto, Naoko Tazawa, Mitsunori Nishikawa, Junji Yamashita, Masanori Takaoka, and Yasuo Matsumura. "A novel and selective Na+/Ca2+ exchange inhibitor, SEA0400, improves ischemia/reperfusion-induced renal injury." European Journal of Pharmacology 478, no. 2-3 (October 2003): 187–98. http://dx.doi.org/10.1016/j.ejphar.2003.08.082.

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15

Egar, J., S. E. Howlett, C. Hancock Friesen, and S. O'Blenes. "112 Impact of SEA0400 as a Cardioplegia Additive in a Novel Cellular Model of Cardioplegic Arrest." Canadian Journal of Cardiology 28, no. 5 (September 2012): S131. http://dx.doi.org/10.1016/j.cjca.2012.07.121.

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16

Nashida, Tetsuaki, Kazuhiro Takuma, Sayoko Fukuda, Toshiyuki Kawasaki, Teisuke Takahashi, Akemichi Baba, Yukio Ago, and Toshio Matsuda. "The specific Na+/Ca2+ exchange inhibitor SEA0400 prevents nitric oxide-induced cytotoxicity in SH-SY5Y cells." Neurochemistry International 59, no. 1 (August 2011): 51–58. http://dx.doi.org/10.1016/j.neuint.2011.03.026.

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17

Chen, Ya, Kevin Payne, Vindya S. Perara, Songping Huang, Akemichi Baba, Toshio Matsuda, and Xin Yu. "Inhibition of the sodium-calcium exchanger via SEA0400 altered manganese-inducedT1changes in isolated perfused rat hearts." NMR in Biomedicine 25, no. 11 (March 21, 2012): 1280–85. http://dx.doi.org/10.1002/nbm.2799.

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18

Nagasawa, Yoshinobu, Bing-Mei Zhu, Jianguang Chen, Kazunori Kamiya, Shigeki Miyamoto, and Keitaro Hashimoto. "Effects of SEA0400, a Na+/Ca2+ exchange inhibitor, on ventricular arrhythmias in the in vivo dogs." European Journal of Pharmacology 506, no. 3 (January 2005): 249–55. http://dx.doi.org/10.1016/j.ejphar.2004.11.011.

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19

Magyar, Janos, Norbert Szentandrássy, Péter Birinyi, Attila Farkas, András Tóth, László Csernoch, András Varró, and Péter P. Nánási. "SEA0400 Fails To Alter The Magnitude Of Intracellular Ca2+ Transients And Contractions In Guinea Pig Heart." Biophysical Journal 96, no. 3 (February 2009): 512a. http://dx.doi.org/10.1016/j.bpj.2008.12.2638.

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20

Waghorn, Ben, Yuhui Yang, Akemichi Baba, Toshio Matsuda, Autumn Schumacher, Nathan Yanasak, and Tom C. C. Hu. "Assessing manganese efflux using SEA0400 and cardiac T 1 -mapping manganese-enhanced MRI in a murine model." NMR in Biomedicine 22, no. 8 (July 10, 2009): 874–81. http://dx.doi.org/10.1002/nbm.1414.

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21

Takahashi, Teisuke, Kenzo Takahashi, Michihito Onishi, Taizo Suzuki, Yu Tanaka, Tomomi Ota, Shigeru Yoshida, Shiro Nakaike, Toshio Matsuda, and Akemichi Baba. "Effects of SEA0400, a novel inhibitor of the Na+/Ca2+ exchanger, on myocardial stunning in anesthetized dogs." European Journal of Pharmacology 505, no. 1-3 (November 2004): 163–68. http://dx.doi.org/10.1016/j.ejphar.2004.10.030.

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22

Ago, Yukio, Toshiyuki Kawasaki, Tetsuaki Nashida, Yuki Ota, Yana Cong, Mari Kitamoto, Teisuke Takahashi, Kazuhiro Takuma, and Toshio Matsuda. "SEA0400, a specific Na+/Ca2+ exchange inhibitor, prevents dopaminergic neurotoxicity in an MPTP mouse model of Parkinson’s disease." Neuropharmacology 61, no. 8 (December 2011): 1441–51. http://dx.doi.org/10.1016/j.neuropharm.2011.08.041.

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23

Nagano, Takayuki, Masakazu Osakada, Yukio Ago, Yutaka Koyama, Akemichi Baba, Sadaaki Maeda, Motohiko Takemura, and Toshio Matsuda. "SEA0400, a specific inhibitor of the Na+ -Ca2+ exchanger, attenuates sodium nitroprusside-induced apoptosis in cultured rat microglia." British Journal of Pharmacology 144, no. 5 (March 2005): 669–79. http://dx.doi.org/10.1038/sj.bjp.0706104.

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24

Birinyi, P., A. Toth, I. Jona, K. Acsai, J. Almassy, N. Nagy, J. Prorok, et al. "The Na+/Ca2+ exchange blocker SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in canine ventricular cardiomyocytes." Cardiovascular Research 78, no. 3 (January 24, 2008): 476–84. http://dx.doi.org/10.1093/cvr/cvn031.

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25

Tanaka, Hikaru, Iyuki Namekata, Kentaro Takeda, Akihiro Kazama, Yoshiko Shimizu, Rina Moriwaki, Wataru Hirayama, Akira Sato, Toru Kawanishi, and Koki Shigenobu. "Unique excitation–contraction characteristics of mouse myocardium as revealed by SEA0400, a specific inhibitor of Na+–Ca2+ exchanger." Naunyn-Schmiedeberg's Archives of Pharmacology 371, no. 6 (June 2005): 526–34. http://dx.doi.org/10.1007/s00210-005-1051-9.

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26

Szentandrássy, Norbert, Péter Birinyi, Gyula Szigeti, Attila Farkas, János Magyar, András Tóth, László Csernoch, András Varró, and Péter P. Nánási. "SEA0400 fails to alter the magnitude of intracellular Ca2+ transients and contractions in Langendorff-perfused guinea pig heart." Naunyn-Schmiedeberg's Archives of Pharmacology 378, no. 1 (May 6, 2008): 65–71. http://dx.doi.org/10.1007/s00210-008-0296-5.

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27

Yatabe, Midori Sasaki, Junichi Yatabe, Kozue Takano, Hironobu Sanada, Junko Kimura, and Tsuyoshi Watanabe. "Effects of renal Na+/Ca2+ exchanger 1 inhibitor (SEA0400) treatment on electrolytes, renal function and hemodynamics in rats." Clinical and Experimental Nephrology 19, no. 4 (November 20, 2014): 585–90. http://dx.doi.org/10.1007/s10157-014-1053-3.

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28

Takahashi, Kenzo, Teisuke Takahashi, Taizo Suzuki, Michihito Onishi, Yu Tanaka, Akiko Hamano-Takahashi, Tomomi Ota, Kazuya Kameo, Toshio Matsuda, and Akemichi Baba. "Protective effects of SEA0400, a novel and selective inhibitor of the Na+/Ca2+ exchanger, on myocardial ischemia–reperfusion injuries." European Journal of Pharmacology 458, no. 1-2 (January 2003): 155–62. http://dx.doi.org/10.1016/s0014-2999(02)02732-2.

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29

Toth, Andras, Peter Birinyi, Karoly Acsai, Norbert Nagy, Janos Prorok, Norbert Szentandrassy, Janos Magyar, Peter P. Nanasi, Julius Gy Papp, and Andras Varro. "The Na+/Ca2+ exchange inhibitor SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in isolated canine ventricular myocytes." FASEB Journal 22, S2 (April 2008): 635. http://dx.doi.org/10.1096/fasebj.22.2_supplement.635.

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30

Yoshiyama, Minoru, Yasuhiro Nakamura, Takashi Omura, Tetsuya Hayashi, Yasuhiro Takagi, Takao Hasegawa, Hiroki Nishioka, Kazuhide Takeuchi, Hiroshi Iwao, and Junichi Yoshikawa. "Cardioprotective Effect of SEA0400, a Selective Inhibitor of the Na+/Ca2+ Exchanger, on Myocardial Ischemia-Reperfusion Injury in Rats." Journal of Pharmacological Sciences 95, no. 2 (2004): 196–202. http://dx.doi.org/10.1254/jphs.fpj03101x.

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31

Namekata, Iyuki, Yayoi Tsuneoka, Akira Takahara, Hideaki Shimada, Takahiko Sugimoto, Kiyoshi Takeda, Midori Nagaharu, Koki Shigenobu, Toru Kawanishi, and Hikaru Tanaka. "Involvement of the Na+/Ca2+ Exchanger in the Automaticity of Guinea-Pig Pulmonary Vein Myocardium as Revealed by SEA0400." Journal of Pharmacological Sciences 110, no. 1 (2009): 111–16. http://dx.doi.org/10.1254/jphs.08159sc.

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32

Feng, Niu Chun, Hiroshi Satoh, Tsuyoshi Urushida, Hideki Katoh, Hajime Terada, Yasuhide Watanabe, and Hideharu Hayashi. "A Selective Inhibitor of Na+/Ca2+ Exchanger, SEA0400, Preserves Cardiac Function and High-Energy Phosphates against Ischemia/Reperfusion Injury." Journal of Cardiovascular Pharmacology 47, no. 2 (February 2006): 263–70. http://dx.doi.org/10.1097/01.fjc.0000202561.69291.ac.

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Namekata, Iyuki, Hideki Nakamura, Hideaki Shimada, Hikaru Tanaka, and Koki Shigenobu. "Cardioprotection without cardiosuppression by SEA0400, a novel inhibitor of Na+-Ca2+ exchanger, during ischemia and reperfusion in guinea-pig myocardium." Life Sciences 77, no. 3 (June 2005): 312–24. http://dx.doi.org/10.1016/j.lfs.2004.10.065.

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34

Tanaka, Hikaru, Hideaki Shimada, Iyuki Namekata, Toru Kawanishi, Naoko Iida-Tanaka, and Koki Shigenobu. "Involvement of the Na+/Ca2+ Exchanger in Ouabain-Induced Inotropy and Arrhythmogenesis in Guinea-Pig Myocardium as Revealed by SEA0400." Journal of Pharmacological Sciences 103, no. 2 (2007): 241–46. http://dx.doi.org/10.1254/jphs.fp0060911.

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35

Lee, Candace, Neeraj S. Visen, Naranjan S. Dhalla, Hoa Dinh Le, Michael Isaac, Platon Choptiany, Gil Gross, et al. "Inhibitory Profile of SEA0400 [2-[4-[(2,5-Difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline] Assessed on the Cardiac Na+-Ca2+ Exchanger, NCX1.1." Journal of Pharmacology and Experimental Therapeutics 311, no. 2 (July 1, 2004): 748–57. http://dx.doi.org/10.1124/jpet.104.070805.

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36

Birinyi, Péter, Károly Acsai, Tamás Bányász, András Tóth, Balázs Horváth, László Virág, Norbert Szentandrássy, et al. "Effects of SEA0400 and KB-R7943 on Na+/Ca2+ exchange current and L-type Ca2+ current in canine ventricular cardiomyocytes." Naunyn-Schmiedeberg's Archives of Pharmacology 372, no. 1 (July 2005): 63–70. http://dx.doi.org/10.1007/s00210-005-1079-x.

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37

Waghorn, B., Y. Yang, B. Klein, A. Baba, T. Matsuda, N. Yanasak, and T. Hu. "TU-D-332-04: Modulating Mn2+ Efflux with SEA0400, Using Cardiac Manganese-Enhanced MRI (MEMRI) T1-Mapping in a Murine Model." Medical Physics 35, no. 6Part21 (June 2008): 2906. http://dx.doi.org/10.1118/1.2962595.

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38

Matsuda, Toshio, Yutaka Koyama, and Akemichi Baba. "Functional Proteins Involved in Regulation of Intracellular Ca2+ for Drug Development: Pharmacology of SEA0400, a Specific Inhibitor of the Na+-Ca2+ Exchanger." Journal of Pharmacological Sciences 97, no. 3 (2005): 339–43. http://dx.doi.org/10.1254/jphs.fmj04007x2.

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39

Christ, Torsten, Peter P. Kovács, Karoly Acsai, Michael Knaut, Thomas Eschenhagen, Norbert Jost, András Varró, Erich Wettwer, and Ursula Ravens. "Block of Na + /Ca 2+ exchanger by SEA0400 in human right atrial preparations from patients in sinus rhythm and in atrial fibrillation." European Journal of Pharmacology 788 (October 2016): 286–93. http://dx.doi.org/10.1016/j.ejphar.2016.06.050.

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40

Namekata, Iyuki, Shogo Hamaguchi, Naoko Iida-Tanaka, Taichi Kusakabe, Keisuke Kato, Toru Kawanishi, and Hikaru Tanaka. "Fluorescence Analysis of the Mitochondrial Effect of a Plasmalemmal Na⁺/Ca²⁺ Exchanger Inhibitor, SEA0400, in Permeabilized H9c2 Cardiomyocytes." Biological & Pharmaceutical Bulletin 40, no. 9 (2017): 1551–55. http://dx.doi.org/10.1248/bpb.b17-00079.

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Soma, Shin, Haruhiro Kuwashima, Chiaki Matsumura, and Tomohiko Kimura. "Inhibition by SEA0400, a Selective Inhibitor of Na+/Ca2+ Exchanger, of Na+-Dependent Ca2+ Uptake and Catecholamine Release in Bovine Adrenal Chromaffin Cells." Journal of Pharmacological Sciences 102, no. 1 (2006): 88–95. http://dx.doi.org/10.1254/jphs.fpj06006x.

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Padín, Juan-Fernando, José-Carlos Fernández-Morales, Román Olivares, Stefan Vestring, Juan-Alberto Arranz-Tagarro, Enrique Calvo-Gallardo, Ricardo de Pascual, Luís Gandía, and Antonio G. García. "Plasmalemmal sodium-calcium exchanger shapes the calcium and exocytotic signals of chromaffin cells at physiological temperature." American Journal of Physiology-Cell Physiology 305, no. 2 (July 15, 2013): C160—C172. http://dx.doi.org/10.1152/ajpcell.00016.2013.

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The activity of the plasmalemmal Na+/Ca2+ exchanger (NCX) is highly sensitive to temperature. We took advantage of this fact to explore here the effects of the NCX blocker KB-R7943 (KBR) at 22 and 37°C on the kinetics of Ca2+ currents ( ICa), cytosolic Ca2+ ([Ca2+]c) transients, and catecholamine release from bovine chromaffin cells (BCCs) stimulated with high K+, caffeine, or histamine. At 22°C, the effects of KBR on those parameters were meager or nil. However, at 37°C whereby the NCX is moving Ca2+ at a rate fivefold higher than at 22°C, various of the effects of KBR were pronounced, namely: 1) no effects on ICa; 2) reduction of the [Ca2+]c transient amplitude and slowing down of its rate of clearance; 3) blockade of the K+-elicited quantal release of catecholamine; 4) blockade of burst catecholamine release elicited by K+; 5) no effect on catecholamine release elicited by short K+ pulses (1–2 s) and blockade of the responses produced by longer K+ pulses (3–5 s); and 6) potentiation of secretion elicited by histamine or caffeine. Furthermore, the more selective NCX blocker SEA0400 also potentiated the secretory responses to caffeine. The results suggest that at physiological temperature the NCX substantially contributes to shaping the kinetics of [Ca2+]c transients and the exocytotic responses elicited by Ca2+ entry through Ca2+ channels as well as by Ca2+ release from the endoplasmic reticulum.

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Takei, Gen L., and Masakatsu Fujinoki. "Regulation of hamster sperm hyperactivation by extracellular Na+." Reproduction 151, no. 6 (June 2016): 589–603. http://dx.doi.org/10.1530/rep-15-0367.

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Abstract Mammalian sperm motility has to be hyperactivated to be fertilization-competent. Hyperactivation is regulated by extracellular environment. Osmolality of mammalian semen is higher than that in female reproductive tract; however, the effect of them on hyperactivation has not been investigated. So we investigated the effect of osmotic environment on hyperactivation using hamster spermatozoa at first. Increase in the osmolality of the media (∼370 mOsm) by increasing the concentration of NaCl (∼150 mmol/L) caused the delay of the expression of hyperactivation. When NaCl concentration varied in the same range (75–150 mmol/L) whereas the osmolality was fixed at 370 mOsm by adding mannitol, the delay of hyperactivation occurred dependent on NaCl concentration. Increase in NaCl concentration also caused suppression of curvilinear velocity, bend angle, and sliding velocity of the flagellum at the onset of incubation, suggesting that NaCl concentration affect both activation and hyperactivation in hamster spermatozoa. Hamster sperm intracellular Ca2+ concentration decreased as extracellular NaCl concentration increased, whereas membrane potential and intracellular pH were unaffected by extracellular NaCl concentration. SN-6 and SEA0400, inhibitors of Na+-Ca2+ exchanger (NCX), increased intracellular Ca2+ and accelerated hyperactivation in the presence of 150 mmol/L NaCl. Tyrosine phosphorylation on fibrous sheath proteins was unaffected by extracellular NaCl concentration. These results suggest that extracellular Na+ suppresses hamster sperm hyperactivation by reducing intracellular Ca2+ via an action of NCX in a tyrosine phosphorylation-independent manner. It seems that the removal of suppression by extracellular Na+ leads to the expression of hyperactivated motility.

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Wolfes, Julian, Christian Ellermann, Niklas Broer, Benjamin Rath, Kevin Willy, Patrick Leitz, Philipp Lange, Lars Eckardt, and Gerrit Frommeyer. "Antiarrhythmic Effect of Ranolazine in Combination with Selective NCX-Inhibition in an Experimental Model of Atrial Fibrillation." Pharmaceuticals 13, no. 10 (October 20, 2020): 321. http://dx.doi.org/10.3390/ph13100321.

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The aim of this study was to investigate the effects of a combination of ranolazine with different selective inhibitors of the Na+/Ca2+-exchanger (NCX) in an established experimental model of atrial fibrillation (AF). Eighteen hearts of New Zealand white rabbits were retrogradely perfused. Atrial catheters were used to record monophasic action potentials (aPRR). Hearts were paced at three different cycle lengths. Thereby, atrial action potential durations (aAPD90), atrial effective refractory periods (aERP) and atrial post-repolarization refractoriness were obtained. Isoproterenol and acetylcholine were employed to increase the occurrence of AF. Thereafter, the hearts were assigned to two groups (n = 9 each group) and additionally perfused with a combination of 10 µM ranolazine and 1 µM of the selective NCX-inhibitor ORM-10103 (group A: Rano-ORM) or 10 µM ranolazine and 1 µM of another NCX-inhibitor, SEA0400 (group B: Rano-SEA). The infusion of Iso/ACh led to a shortening of aAPD90, aERP, aPRR and the occurrence of AF episodes was significantly increased. Additional perfusion with ranolazine and ORM-10103 (group A) significantly prolonged the refractory periods and aPRR and AF episodes were effectively reduced. In group B, Rano-SEA led to a slight decrease in aAPD90 while aERP and aPRR were prolonged. The occurrence of AF episodes was consecutively reduced. To our knowledge, this is the first study investigating the effect of ranolazine combined with different selective NCX-inhibitors in an isolated whole-heart model of AF. Both combinations prolonged aERP and aPRR and thereby suppressed the induction of AF.

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Lemme, Marta, Ingke Braren, Maksymilian Prondzynski, Bülent Aksehirlioglu, Bärbel M. Ulmer, Mirja L. Schulze, Djemail Ismaili, et al. "Chronic intermittent tachypacing by an optogenetic approach induces arrhythmia vulnerability in human engineered heart tissue." Cardiovascular Research 116, no. 8 (October 9, 2019): 1487–99. http://dx.doi.org/10.1093/cvr/cvz245.

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Abstract Aims Chronic tachypacing is commonly used in animals to induce cardiac dysfunction and to study mechanisms of heart failure and arrhythmogenesis. Human induced pluripotent stem cells (hiPSC) may replace animal models to overcome species differences and ethical problems. Here, 3D engineered heart tissue (EHT) was used to investigate the effect of chronic tachypacing on hiPSC-cardiomyocytes (hiPSC-CMs). Methods and results To avoid cell toxicity by electrical pacing, we developed an optogenetic approach. EHTs were transduced with lentivirus expressing channelrhodopsin-2 (H134R) and stimulated by 15 s bursts of blue light pulses (0.3 mW/mm2, 30 ms, 3 Hz) separated by 15 s without pacing for 3 weeks. Chronic optical tachypacing did not affect contractile peak force, but induced faster contraction kinetics, shorter action potentials, and shorter effective refractory periods. This electrical remodelling increased vulnerability to tachycardia episodes upon electrical burst pacing. Lower calsequestrin 2 protein levels, faster diastolic depolarization (DD) and efficacy of JTV-519 (46% at 1 µmol/L) to terminate tachycardia indicate alterations of Ca2+ handling being part of the underlying mechanism. However, other antiarrhythmic compounds like flecainide (69% at 1 µmol/L) and E-4031 (100% at 1 µmol/L) were also effective, but not ivabradine (1 µmol/L) or SEA0400 (10 µmol/L). Conclusion We demonstrated a high vulnerability to tachycardia of optically tachypaced hiPSC-CMs in EHT and the effective termination by ryanodine receptor stabilization, sodium or hERG potassium channel inhibition. This new model might serve as a preclinical tool to test antiarrhythmic drugs increasing the insight in treating ventricular tachycardia.

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Miura, Masahito, Taiki Hattori, Naomi Murai, Tsuyoshi Nagano, Taichi Nishio, Penelope A. Boyden, and Chiyohiko Shindoh. "Regional increase in extracellular potassium can be arrhythmogenic due to nonuniform muscle contraction in rat ventricular muscle." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 11 (June 1, 2012): H2301—H2309. http://dx.doi.org/10.1152/ajpheart.01161.2011.

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In the ischemic myocardium, extracellular potassium ([K+]o) increases to ≥20 mmol/l. To determine how lethal arrhythmias occur during ischemia, we investigated whether the increased spatial pattern of [K+]o, i.e., a regional or a global increase, affects the incidence of arrhythmias. Force, sarcomere length, membrane potential, and nonuniform intracellular Ca2+ ([Ca2+]i) were measured in rat ventricular trabeculae. A “regional” or “global” increase in [K+]o was produced by exposing a restricted region of muscle to a jet of 30 mmol/l KCl or by superfusing trabeculae with a solution containing 30 mmol/l KCl, respectively. The increase in [Ca2+]i (CaCW) during Ca2+ waves was measured (24°C, 3.0 mmol/l [Ca2+]o). A regional increase in [K+]o caused nonuniform [Ca2+]i and contraction. In the presence of isoproterenol, the regional increase in [K+]o induced sustained arrhythmias in 10 of 14 trabeculae, whereas the global increase did not induce such arrhythmias. During sustained arrhythmias, Ca2+ surged within the jet-exposed region. In the absence of isoproterenol, the regional increase in [K+]o increased CaCW, whereas the global increase decreased it. This increase in CaCW with the regional increase in [K+]o was not suppressed by 100 μmol/l streptomycin, whereas it was suppressed by 1) a combination of 10 μmol/l cilnidipine and 3 μmol/l SEA0400; 2) 20 mmol/l 2,3-butanedione monoxime; and 3) 10 μmol/l blebbistatin. A regional but not a global increase in [K+]o induces sustained arrhythmias, probably due to nonuniform excitation-contraction coupling. The same mechanism may underlie arrhythmias during ischemia.

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Amran, Md Shah, Keitaro Hashimoto, and Nobuo Homma. "Effects of Sodium-Calcium Exchange Inhibitors, KB-R7943 and SEA0400, on Aconitine-Induced Arrhythmias in Guinea Pigs in Vivo, in Vitro, and in Computer Simulation Studies." Journal of Pharmacology and Experimental Therapeutics 310, no. 1 (March 17, 2004): 83–89. http://dx.doi.org/10.1124/jpet.104.066951.

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An, Jianzhong, Samhita S. Rhodes, Ming Tao Jiang, Zeljko J. Bosnjak, Ming Tian, and David F. Stowe. "Anesthetic Preconditioning Enhances Ca2+Handling and Mechanical and Metabolic Function Elicited by Na+–Ca2+Exchange Inhibition in Isolated Hearts." Anesthesiology 105, no. 3 (September 1, 2006): 541–49. http://dx.doi.org/10.1097/00000542-200609000-00018.

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Background Anesthetic preconditioning (APC) is well known to protect against myocardial ischemia-reperfusion injury. Studies also show the benefit of Na+-Ca2+ exchange inhibition on ischemia-reperfusion injury. The authors tested whether APC plus Na+-Ca2+ exchange inhibitors given just on reperfusion affords additive protection in intact hearts. Methods Cytosolic [Ca2+] was measured by fluorescence at the left ventricular wall of guinea pig isolated hearts using indo-1 dye. Sarcoplasmic reticular Ca2+-cycling proteins, i.e., Ca2+ release channel (ryanodine receptor [RyR2]), sarcoplasmic reticular Ca2+-pump adenosine triphosphatase (SERCA2a), and phospholamban were measured by Western blots. Hearts were assigned to seven groups (n = 8 each): (1) time control; (2) ischemia; (3, 4) 10 microM Na+-Ca2+ exchange inhibitor KB-R7943 (KBR) or 1 microM SEA0400 (SEA), given during the first 10 min of reperfusion; (5) APC initiated by sevoflurane (2.2%, 0.41 +/- 0.03 mm) given for 15 min and washed out for 15 min before ischemia-reperfusion; (6, 7) APC plus KBR or SEA. Results The authors found that APC reduced the increase in systolic [Ca2+], whereas KBR and SEA both reduced the increase in diastolic [Ca2+] on reperfusion. Each intervention improved recovery of left ventricular function. Moreover, APC plus KBR or SEA afforded better functional recovery than APC, KBR, or SEA alone (P < 0.05). Ischemia-reperfusion-induced degradation of major sarcoplasmic reticular Ca2+-cycling proteins was attenuated by APC, but not by KBR or SEA. Conclusions APC plus Na+-Ca2+ exchange inhibition exerts additive protection in part by reducing systolic and diastolic Ca2+ overload, respectively, during ischemia-reperfusion. Less degradation of sarcoplasmic reticular Ca2+-cycling proteins may also contribute to cardiac protection.

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Pandit, Meghana M., Kevin A. Strait, Toshio Matsuda, and Donald E. Kohan. "Na delivery and ENaC mediate flow regulation of collecting duct endothelin-1 production." American Journal of Physiology-Renal Physiology 302, no. 10 (May 15, 2012): F1325—F1330. http://dx.doi.org/10.1152/ajprenal.00034.2012.

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Collecting duct (CD) endothelin-1 (ET-1) is an important autocrine inhibitor of Na and water transport. CD ET-1 production is stimulated by extracellular fluid volume expansion and tubule fluid flow, suggesting a mechanism coupling CD Na delivery and ET-1 synthesis. A mouse cortical CD cell line, mpkCCDc14, was subjected to static or flow conditions for 2 h at 2 dyn/cm2, followed by determination of ET-1 mRNA content. Flow with 300 mosmol/l NaCl increased ET-1 mRNA to 65% above that observed under static conditions. Increasing perfusate osmolarity to 450 mosmol/l with NaCl or Na acetate increased ET-1 mRNA to ∼184% compared with no flow, which was not observed when osmolarity was increased using mannitol or urea. Reducing Na concentration to 150 mosmol/l while maintaining total osmolarity at 300 mosmol/l with urea or mannitol decreased the flow response. Inhibition of epithelial Na channel (ENaC) with amiloride or benzamil abolished the flow response, suggesting involvement of ENaC in flow-regulated ET-1 synthesis. Aldosterone almost doubled the flow response. Since Ca2+ enhances CD ET-1 production, the involvement of plasma membrane and mitochondrial Na/Ca2+ exchangers (NCX) was assessed. SEA0400 and KB-R7943, plasma membrane NCX inhibitors, did not affect the flow response. However, CGP37157, a mitochondrial NCX inhibitor, abolished the response. In summary, the current study indicates that increased Na delivery, leading to ENaC-mediated Na entry and mitochondrial NCX activity, is involved in flow-stimulated CD ET-1 synthesis. This constitutes the first report of either ENaC or mitochondrial NCX regulation of an autocrine factor in any biologic system.

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Hohendanner, Felix, Senka Ljubojević, Niall MacQuaide, Michael Sacherer, Simon Sedej, Liesbeth Biesmans, Paulina Wakula, et al. "Intracellular Dyssynchrony of Diastolic Cytosolic [Ca 2+ ] Decay in Ventricular Cardiomyocytes in Cardiac Remodeling and Human Heart Failure." Circulation Research 113, no. 5 (August 16, 2013): 527–38. http://dx.doi.org/10.1161/circresaha.113.300895.

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Rationale : Synchronized release of Ca 2+ into the cytosol during each cardiac cycle determines cardiomyocyte contraction. Objective: We investigated synchrony of cytosolic [Ca 2+ ] decay during diastole and the impact of cardiac remodeling. Methods and Results: Local cytosolic [Ca 2+ ] transients (1-µm intervals) were recorded in murine, porcine, and human ventricular single cardiomyocytes. We identified intracellular regions of slow (slowCaR) and fast (fastCaR) [Ca 2+ ] decay based on the local time constants of decay (TAU local ). The SD of TAU local as a measure of dyssynchrony was not related to the amplitude or the timing of local Ca 2+ release. Stimulation of sarcoplasmic reticulum Ca 2+ ATPase with forskolin or istaroxime accelerated and its inhibition with cyclopiazonic acid slowed TAU local significantly more in slowCaR, thus altering the relationship between SD of TAU local and global [Ca 2+ ] decay (TAU global ). Na + /Ca 2+ exchanger inhibitor SEA0400 prolonged TAU local similarly in slowCaR and fastCaR. FastCaR were associated with increased mitochondrial density and were more sensitive to the mitochondrial Ca 2+ uniporter blocker Ru360. Variation in TAU local was higher in pig and human cardiomyocytes and higher with increased stimulation frequency (2 Hz). TAU local correlated with local sarcomere relengthening. In mice with myocardial hypertrophy after transverse aortic constriction, in pigs with chronic myocardial ischemia, and in end-stage human heart failure, variation in TAU local was increased and related to cardiomyocyte hypertrophy and increased mitochondrial density. Conclusions: In cardiomyocytes, cytosolic [Ca 2+ ] decay is regulated locally and related to local sarcomere relengthening. Dyssynchronous intracellular [Ca 2+ ] decay in cardiac remodeling and end-stage heart failure suggests a novel mechanism of cellular contractile dysfunction.

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