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Relevant bibliographies by topics / SEA0400

Academic literature on the topic 'SEA0400'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "SEA0400"

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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Dissertations / Theses on the topic "SEA0400"

1

Bauer, Klemens Verfasser], and Christian [Akademischer Betreuer] [Pott. "Einfluss des Natrium-Kalzium-Austauscher (NCX1)-Antagonisten SEA0400 auf Kalzium-Handling und Arrhythmogenese in Abhängigkeit vom NCX1-Expressionsniveau / Klemens Bauer ; Betreuer: Christian Pott." Münster : Universitäts- und Landesbibliothek Münster, 2016. http://d-nb.info/1141577461/34.

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2

Zhao, Jun, and e52677@ems rmit edu au. "The functional study of Na+/Ca2+ exchanger in vascular smooth muscle cells." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080617.163746.

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Na+/Ca2+ exchanger (NCX) is a membrane protein which can mediate either Ca2+ entry (reverse mode) or exit (forward mode) in cells. As one of the major Ca2+ transport systems, NCX is postulated to play a critical role in the vascular smooth muscle cell. The aims of the present study are to firstly demonstrate the functional existence of NCX in vascular smooth muscle (including aorta and arteriole); to clarify the modulation of NCX; to explore the selectivity of NCX inhibitor KB-R7943; and lastly to investigate the role of NCX in the myogenic response. KB-R7943 has been widely used as a NCX inhibitor. The study investigated its pharmacological actions in rat aorta on a variety of Ca2+ dependent systems. Rat aortic rings were used. The constriction to low extracellular [Na+] is a functional response mediated by NCX operating in reverse mode. The data demonstrate that 10 µM KB-R7943 inhibited L-type Ca2+ channel, the capacitative Ca2+ entry and  adrenergic receptor pathway. Nevertheless, KB-R7943 can be used as a selective inhibitor of NCX at the lower concentration of 1 µM in rat aortic rings. The study investigated whether the endothelium could modulate NCX in rat aortic rings. Lowering extracellular [Na+] to 1.18 mM induced constriction in endothelium denuded rat aortic rings, but only a small constriction in endothelium intact rat aortic rings. In endothelium intact rat aortic rings, the guanylate cyclise inhibitor ODQ (1 µM) and the nitric oxide synthase inhibitor L-NAME (50 µM) greatly amplified the vasoconstriction to lowering extracellular [Na+], but had no effect when the endothelium was removed. The adenylate cyclise inhibitor SQ 22536 (100 µM) and the cyclooxygenase inhibitor indomethacin (10 M) showed no significant effect on the low-Na+ induced vasoconstriction in either endothelium denuded or intact aortic rings. The results suggest that endothelium modulated the NCX operation via the nitric oxide/guanylate cyclase, not the adenylate cyclase system; further prostanoids including prostacyclin was not involved. The interaction between nitric oxide and NCX was furt her explored using the nitric oxide donor sodium nitroprusside. Endothelium denuded rat aortic rings were preconstricted to the same extent with either low Na+ (1.18 mM), or the thromboxane A2 agonist U46619 (0.1 µM) or high K+ (80 mM). The vasorelaxation of SNP (30 nM) in low Na+ constriction was significantly larger compared to other agents. This indicates that NO has a special antagonism of low Na+ constriction and a hypothesis is proposed involving Na+/K+ ATPase. The investigation of NCX is mainly conducted in large vessels; much less evidence is available for small resistance vessels. The study investigated the role of NCX on myogenic response in pressurized cremaster muscle arterioles. Reducing extracellular [Na+] resulted in graded vasoconstriction which was inhibited by NCX inhibitor SEA0400 (1 µM). Myogenic vasoconstriction and the concomitant rise in internal [Ca2+] were induced by a transmural pressure increase from 70 to 120 mmHg which was prevented by NCX inhibitor: SEA0400 (1 µM). In conclusion, the present study suggests that NCX contributes to the myogenic response in cremaster arteriole.

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3

Egar, Jeanne. "Cardioprotective effect of Na+/Ca2+ exchange inhibition in cardioplegic arrest by SEA0400." 2013. http://hdl.handle.net/10222/35431.

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This study investigated the effects of SEA0400, a Na+/Ca2+ exchange inhibitor, in cardioplegia on rat myocyte contractile function. SEA0400 significantly reduced the accumulation of diastolic Ca2+ throughout cardioplegic arrest compared to ischemic control and cardioplegia. Cells treated with SEA0400 during cardioplegic arrest showed significantly larger Ca2+ transient amplitudes and contractions throughout reperfusion compared to cells treated with cardiopelgia alone. Intracellular Ca2+ stores were similar in both cardioplegic groups at baseline and during reperfusion. Together these results suggest that SEA0400 has beneficial effects at protecting ventricular myocytes during cardioplegic arrest and that SEA0400 in cardioplegia may affect myofilament Ca2+ sensitivity.

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4

Choptiany, Markian Platon. "Effects of SEA0400 on mutant NCX1.1 Na+-Ca2+ exchangers with altered ionic regulation." 2004. http://hdl.handle.net/1993/15808.

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5

Lee, Candace Y. W. "Evaluation of a novel sodium-calcium exchange inhibitor, SEA0400, in the JCR:LA-cp rat, a model of the metabolic syndrome and cardiovascular disease." 2005. http://hdl.handle.net/1993/20171.

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