Amiodarone Modulation of Intracellular Transport of Calcium Ions in Cardiomyocites

Abstract

The influence of amiodarone on intracellular transport of calcium ion in cardiomyocytes of rat was investigated. The experiments were performed on isolated papillary muscles of Wistar rats. Force-frequency dependence (0.7, 1, 2, 3, 4 Hz), extrasystolic and postextrasystolic contractions and post-rest (4-60 s) reactions of rat myocardium after amiodarone treatment (1 μM) were investigated. Decay potentiation coefficient of contraction force was estimated. Results. The analyses of force-frequency dependence has shown that amiodarone prevent the decreasing of the force contraction at increasing of the stimulation frequency. Amiodarone promotes increase of the time constant t1(T50), that indicate the drug promotes acceleration of Са2+ transport inside the SR resulting increase of Са2+ in the places of its release from the sarcoplasmic reticulum (SR). Treatment of papillary muscle with amiodarone decreased amplitude of extrasystolic contractions. As known, postextrasystolic and post-rest reactions of myocardium characterize the SR function. We have found amiodarone increased potentiation of postextrasystolic and post-rest contractions. Preliminary caffeine perfusion of muscles preparations cancelled the amiodarone-induced increasing postextrasystolic and post-rest potentiation. However, potentiation decay coefficient before and after treatment with amiodarone didn’t have difference. Conclusions, amiodarone influences on intracellular calcium ions homeostasis by modulation SR functions related with most likely are stipulated either by activation of Са2+ transport from uptake sites to release sites or by prevent of Са2+ leakage from the SR.

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D. Kondratyeva, S. Afanasiev, S. Popov and R. Batalov, "Amiodarone Modulation of Intracellular Transport of Calcium Ions in Cardiomyocites," Pharmacology & Pharmacy, Vol. 3 No. 3, 2012, pp. 307-315. doi: 10.4236/pp.2012.33041.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] S.J. Connolly, “Evidence-Based Analysis of Amiodarone Efficacy and Safety”, Circulation, Vol. 100, 1999, pp. 2025-2034.
[2] L.M. Letelier, K. Udol, J. Ena, B. Weaver and G.H. Guyatt, “Effectiveness of amiodarone for conversion of atrial fibrillation to sinus rhythm: a meta-analysis”, Archives of Internal Medicine, Vol. 163, No 7, 2003, pp. 777-785.
[3] R.f. Bosch, g. li, r. gaspo and s. nattel, “Electrophysiologic Effects of Chronic Amiodarone Therapy and Hypothyroidism, Alone and in Combination, on Guinea Pig Ventricular Myocytes”, The Journal Pharmacology and Experimental Therapeutics, Vol. 289, No. 1, 1999, pр. 156-165.
[4] K. Kamiya, A. Nishiyama, K. Yasui, M. Hojo, M.C. Sanguinetti and I. Kodama, “Short-and Long-Term Effects of Amiodarone on the Two Components of Cardiac Delayed Rectifier K+ Current”, Circulation, Vol. 103, 2001, pp. 1317-1324.
[5] M.D. Freedman and J.C. Somberg, “Pharmacology and pharmacokinetics of amiodarone”, Journal of Clinical Pharmacology, Vol. 31, 1991, pp. 1061-1069.
[6] I. Kodama, K. Kamiya and J. Toyama, “Cellular electropharmacology of amiodarone” Cardiovascular Research, Vol. 35, No 1, 1997, pp. 13-29.
[7] I. Kodama, K. Kamiya, Honjo H. and J. Toyama, “Acute and chronic effects of amiodarone on mammalian ventricular cells”, Japanese Heart Journal, Vol. 37, No 5, 1996 pp. 719-730.
[8] P. Chatelain, L. Meysmans, J.R. Mattéazzi, P. Beaufort and M. Clinet, “Interaction of the antiarrhythmic agents SR 33589 and amiodarone with the beta-adrenoceptor and adenylate cyclase in rat heart”, British Journal of Pharmacology, Vol. 116, No 3, 1995, pp. 1949-1956.
[9] V. Drvota, J. Haggblad, I. Blange, Y. Magnusson and S. Sylvén, “The effect of amiodarone on the beta-adrenergic receptor is due to a downregulation of receptor protein and not to a receptor-ligand interaction”, Biochemical and Biophysical Research Communications, Vol. 255 (2), 1999, pp. 515-520.
[10] P. Schnabel, F. Mies, C. Maack, S. Rosenkranz, O. Zolk and M.Bohm, “Beneficial effects of amiodarone in heart failure: interaction with beta-adrenoceptors rather than G proteins”, European Journal of Pharmacology, Vol. 369 (3), 1999, pp. 391-394.
[11] D.P. Zankov, W.G. Ding, H. Matsuura and M. Horie, “Open-state unblock characterizes acute inhibition of I potassium current by amiodarone in guinea pig ventricular myocytes” Journal of Cardiovascular Electrophysiology, Vol. 16 (3), 2005, pp. 314-322.
[12] M.E. D′?az, H.K. Grahama, S.C. O’Neill, A.W. Trafford, D.A. Eisner, “The control of sarcoplasmic reticulum Ca content in cardiac muscle”, Cell Calcium, Vol. 38 (3-4), 2005, pp. 391–396.
[13] A.M. Prasad and G. Inesi, “Analysis of calcium transients in cardiac myocytes and assessment of the sarcoplasmic reticulum Ca2+-ATPase contribution”, Methods in Molecular Biology, Vol. 798 (6), 2012, pp. 411-421.
[14] A.M. Rubtsov, “Molecular mechanisms of regulation of the activity of sarcoplasmic reticulum Carelease channels (ryanodine receptors), muscle fatigue, and Severin's phenomenon”, Biochemistry (Mosc), Vol. 66, No10, 2001, pp. 1132-1143.
[15] H.E. ter Keurs, “Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback”, Pflugers Archiv, 462, No 1, 2011, pp. 165-175.
[16] A. Zarain-Herzberg, J. Frago-so-Medina and R.Estrada-Avilés, “Calcium-regulated transcriptional pathways in the normal and pathologic heart”, IUBMB Life, Vol. 63 (10), 2011, pp. 847-855.
[17] D.M. Bers, “Calcium cycling and signaling in cardiac myocytes”, Annual Review of Physiology, Vol. 70, 2008, pp. 23-49.
[18] K. Brixius, M. Pietsch., R.H.G. Schwinger, “The intracellular Ca2+-homeostasis influences the frequency-dependent force generation in man”, Basic Research in Cardiology, Vol. 94, 1999, pp. 152-158.
[19] P. Pucelík, “Pharmacological blockade of sarcoplasmic reticulum induces a negative lusitropic effect”, General Physiology & Biophysics, Vol. 26 (3), 2007, pp. 214-220.
[20] D.S. Kondratyeva, S.A. Afanasyev, M.V. Egorova, T.Yu. Rebrova and S.V. Popov, “Contractile activity and energetic metabolism of postinfarction heart against diabetic damage in experiment”, The Siberian Medical Journal, Vol. 26, No2, pp.136-140.
[21] U. Ravens, C. Mahl, A. Ohler, S.M.C. Hardman and M.I.M. Noble, “Mechanical restitution and recirculation fraction in cardiac myocytes and left ventricular muscle of adult rats”, Basic Research in Cardiology, Vol. 91, 1996, pp. 123-130.
[22] S.N. Wu, A.Y. Shen and T.L. Hwang, “Analysis of mechanical restitution and post-rest potentiation in isolated rat atrium”, Chinese Journal of Physiology, Vol. 39, 1996, p. 23-29.
[23] F.D. Marengo, M.T. Marquez, P. Bonazzola and J.E. Ponce-Hornos, “The heart extrasystole: an energetic approach”, American Journal of Physiology, Vol. 276 (1), 1999, pp. H309-H316.
[24] T. Tatsumi, J. Asayama, H. Miyazaki, T. Shirayama, I. Omori, D. Inoue and M. Nakagawa, “The effects of an extra-stimulation on post-extra-systolic potentiation in papillary muscle of rats”, Japanese Heart Journal, Vol. 31(3), 1990, pp. 355-363.
[25] D.V. Vassallo, E.Q. Lima, P. Campagnaro, A.N. Faria and J.G. Mill, “Mechanisms underlying the genesis of post-extrasystolic potentiation in rat cardiac muscle”, Brazilian Journal of Medical & Biological Research, Vol. 28 (3), 1995, pp. 377-383.
[26] J. Mizuno, J. Araki, S. Mohri, H. Minami, Doi Y., W. Fujinaka, K. Miyaji, T. Kiyooka, Y. Oshima, G. Iribe, M. Hirakawa and H. Suga, “Frank-Starling mechanism retains recirculation fraction of myocardial Ca(2+) in the beating heart”, Japanese Journal of Physiology, Vol. 51 (6), pp. 2001, 733-743.
[27] D.M. Bers, “Ca influx and sarcoplasmic reticulum Ca release in cardiac muscle activation during postrest recovery”, American Journal of Physiology, Vol. 248, 1985, pp. H366-H381.
[28] W.F. Bluhm, M. Meyer, E.A. Swanson and W.H. Dillmann, “Postrest potentiation of active force in mouse papillary muscles is greatly accelerated by increased stimulus frequency”, Annals of New York Academy of Sciences, Vol. 853, No, 1998, pp. 304-307.
[29] J. Layland and J.C. Kentish, “Positive force-and [Ca2+]i-frequency relationships in rat ventricular trabeculae at physiological frequencies”, American Journal of Physiology, Vol. 276, 1999, pp.H9–H18.
[30] D.M. Bers, “Excitation–contraction coupling and cardiac force”, Kluwer Academic Publishers, Dordrecht, 2002.
[31] R. A. Bouchard and D. Bose, “Analysis of the interval-force relationship in rat and canine ventricular myocardium”, American Journal of Physiology, Heart and Circulatory Physiology, Vol. 257 (6), 1989, pp. H2036–H2047.
[32] M. Endoh, “Force-frequency relationship in intact mammalian ventricular myocardium: physiological and pathophysiological relevance”, European Journal of Pharmacology, Vol. 500(1-3), 2004, pp.73-86.
[33] Y. Xu, M.M. Monasky, N. Hiranandani, K.M. Haizlip, G.E. Billman and P.M. Janssen, “Effect of Twitch Interval Duration on the Contractile Function of Subsequent Twitches in Isolated Rat, Rabbit, and Dog Myocardium under Physiological Conditions”, Journal of Applied Physiology, Vol. 111 (4), 2011, pp. 1159-1167.
[34] M.M. Monasky and P.M. Janssen, “The positive force-frequency relationship is maintained in absence of sarcoplasmic reticulum function in rabbit, but not in rat myocardium”, Journal of Comparative Physiology, 179(4), 2009, pp. 469-479.
[35] T. Matsushita, M. Okamoto, J. Toyama, I. Kodama, S. Ito, T. Fukutomi, S. Suzuki and M. Itoh, “Adriamycin causes dual inotropic effects through complex modulation of myocardial Ca2+ handling”, Japanese Circulation Journal, Vol.64, No 1, 2000, pp. 65-71.
[36] J. Asayama, T. Tatsumi, H. Miyazaki, I. Omori., D..Inoue and M. Nakagawa, “Suppressing effects of caffeine on postextrasystolic potentiation in papillary muscles of guinea pigs”, Japanese Circulation Journal, Vol. 54, No 2, 1990, pp. 207-213.
[37] M. Porta, A.V. Zima, A, Nani, P.L. Diaz-Sylvester, J.A. Copello, J. Ramos-Franco, L.A. Blatter and M.Fill, “Single ryanodine receptor channel basis of caffeine's action on Ca2+ sparks”, Biophysical Journal, Vol. 100 (4), 2011, 931-938.
[38] R. Zucchi, F.Ronca and S. Ronca-Testoni, “Modulation of sarcoplasmic reticulum function: a new strategy in cardioprotection”, Pharmacology & Therapeutics, Vol. 89, 2001, pp. 47-65.

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