Abstract
Catecholamines have physiologically important effects on the performance of the heart through the activation of adrenergic receptors. In general, it is known that sympathetic nervous system activation modulates the signaling pathway that controls excitation-contraction coupling (ECC) in the heart. Coordinated myocyte handling of Ca2+ is essential for efficient ECC in the heart. A growing body of knowledge on cardiac β-adrenergic receptor (β-AR) signal transduction demonstrates that the agonist-bound β-AR selectively interacts with the stimulatory G protein (Gs), which activates adenylyl cyclase (AC), catalyzing cAMP formation. Subsequently, activation of cAMP-dependent protein kinase A (PKA) leads to phosphorylation of regulatory proteins involved in cardiac ECC and energy metabolism. Published data have shown that the altered cardiac responses in pathological conditions are closely related to the function of the β-AR system. From the current literature it is clear that the β-AR system and its importance in regulating cardiac function under both physiological and pathophysiological situations has attracted the attention of many investigators. Ca2+ functions as a critical second messenger in mediating fast intracellular responses in all tissues through signaling proteins to coordinate cell function with different intracellular mechanisms. In addition, the identification of oxidatively sensitive proteins that modulate intracellular signaling mechanisms and the associated generation of reactive oxygen species (ROS) are critical to understanding how cells respond to oxidative stress. Therefore, any disturbance in the intracellular ionic homeostasis due to the excess ROS, was shown to result in the occurrence of impaired cardiac contractile activity. Since β-ARs and AC are known to participate in the regulation of cardiac function, it is possible that the β-AR-linked signal transduction pathway is also affected by ROS.
Keywords
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Ayaz, M., and Turan, B. 2006. Selenium prevents diabetes-induced alterations in [Zn2+ ]i and met-allothionein level of rat heart via restoration of cell redox cycle. Am. J. Physiol. Heart Circ. Physiol. 290: H1071-H1080.
Ayaz, M., Ozdemir, S., Ugur, M., Vassort, G., and Turan, B. 2004. Effects of selenium on altered mechanical and electrical cardiac activities of diabetic rat. Arch. Biochem. Biophys. 426:83-90.
Ayaz, M., Ozdemir, S., Yaras, N., Vassort, G., and Turan, B. 2005. Selenium-induced alterations in ionic currents of rat cardiomyocytes. Biochem. Biophys. Res. Commun. 327:163-173.
Bettger, W. J. 1993. Zinc and selenium, site-specific versus general antioxidation. Can. J. Pharma-col. 71:721-724.
Bigelow, D. J., and Squier, T. C. 2005. Redox modulation of cellular signaling and metabolism through reversible oxidation of methionine sensors in calcium regulatory proteins. Biochim. Biophys. Acta 1703:121-134.
Bj örnstedt, M., Kumar, S., and Holgren, A. 1995. Selenite and selenodiglutathione. Reactions with thioredoxin systems. Methods Enzymol. 252:209-219.
Bohm, M. 1995. Alterations of beta-adrenoceptor-G-protein-regulated adenylyl cyclase in heart failure. Mol. Cell. Biochem. 147:147-160.
Bohm, M., and Lohse, M. J. 1994. Quantification of beta-adrenoceptors and beta-adrenoceptor kinase on protein and mRNA levels in heart failure. Eur. Heart J. 15:30-34.
Bolli, R., and Marban, E. 1999. Molecular and cellular mechanisms of myocardial stunning. Physiol. Rev. 79:609-634.
Bowie, A., and O’Neill, L. A. 2000. Oxidative stress and nuclear factor kappaB activation: a reassessment of the evidence in the light of recent discoveries. Biochem. Pharmacol. 59:13-23.
Bristow, M. R., Cubicciotti, R., Ginsburg, R., Stinson, E. B., and Johnson, C. 1982. Histamine-mediated adenylate cyclase stimulation in human myocardium. Mol. Pharmacol. 21:671-679.
Brodde, O.-E., Hillemann, S., Kunde, K., Vogesang, M., and Zerkowski, H.-R. 1992. Receptor systems affecting force of contraction in the human heart and their alterations in chronic heart failure. J. Heart Lung Transplant. 11:S164-S174.
Brodde, O.-E., Michel, M. C., and Zerkowski, H.-R. 1995. Signal transduction mechanisms con-trolling cardiac contractility and their alterations in chronic heart failure. Cardiovasc. Res. 30: 570-584.
Cargnoni, A., Ceconi, C., Gaia, G., Agnoletti, L., and Ferrari, R. 2002. Cellular thiols redox sta-tus: a switch for NF-κB activation during myocardial post-ischemic reperfusion. J. Mol. Cell. Cardiol. 34: 997-1005.
Cheng, H. J., Zhang, Z. S., Onishi, K., Ukai, T., Sane, D. C., and Cheng, C. P. 2001. Upregulation of functional beta(3)-adrenergic receptor in the failing canine myocardium. Circ. Res. 89:599-606.
Choi, K. M., Zhong; Y., Hoit, B. D., Grupp, I. L., Hahn, H., Dilly, K. W., Guatimosim, S., Lederer, W. J., and Matlib, M. A. 2002. Defective intracellular Ca(2+) signaling contributes to car-diomyopathy in Type 1 diabetic rats. Am. J. Physiol. Heart Circ. Physiol. 283:H1398-H1408.
Chu, S. H., Sutherland, K., Beck, J., Kowalski, J., Goldspink, P., and Schwertz, D. 2005. Sex differences in expression of calcium-handling proteins and beta-adrenergic receptors in rat heart ventricle. Life Sci. 76:2735-2749.
Coppey, L. J., Gellett, J. S., Davidson, E. P., Dunlap, J. A., Lund, D. D., and Yorek, M. A. 2001. Effect of antioxidant treatment of streptozotocin-induced diabetic rats on endoneurial blood flow, motor nerve conduction velocity, and vascular reactivity of epineurial arterioles of the sciatic nerve. Diabetes 50:1927-1937.
Cruzado, M. C., Risler, N. R., Miatello, R. M., Yao, G., Schiffrin, E. L., and Touyz, R. M. 2005. Vascular smooth muscle cell NAD(P)H oxidase activity during the development of hyperten-sion: effect of angiotensin II and role of insulinlike growth factor-1 receptor transactivation. Am. J. Hypertens. 18:81-87.
Da Ros, R., Assaloni, R., and Ceriello, A. 2004. Antioxidant therapy in diabetic complications: what is new? Curr. Vasc. Pharmacol. 2:335-341.
Das, D. K., Maulik, N., and Engelman, R. M. 2004. Redox regulation of angiotensin II signaling in the heart. J. Cell. Mol. Med. 8(1):144-152.
Das, P. K., Temsah, R., Panagia, V., and Dhalla, N. S. 1997. Beta-adrenergic linked signal trans-duction mechanisms in developing and aging hearts. Heart Fail. Rev. 2:23-41.
Dhalla, N. S., Golfman, L., Takeda, N., and Nagano, M. 1999. Evidence for the role of oxidative stress in acute ischemic heart disease: a brief review. Can. J. Cardiol. 15:587-593.
Dhalla, N. S., Pierce, G. N., Panagia, V., Singal, P. K., and Beamish, R. E. 1982. Calcium move-ments in relation to heart function. Basic Res. Cardiol. 77:117-139.
Dhalla, N. S., Wang, X., Sethi, R., and Das, P. K. 1997. Beta-adrenergic linked signal transduction mechanisms in failing heart. Heart Fail. Rev. 2:55-65.
Eisner, D. A., Trafford, A. W., Diaz, M. E., Overend, C. L., and O’Neill, S. C. 1998. The con-trol of Ca release from the cardiac sarcoplasmic reticulum: regulation versus autoregulation. Cardiovasc. Res. 38:589-604.
Eley, D. W., Eley, J. M., Korecky, B., Fliss, H., and Desilets, M. 1991. Calcium homeostasis in rabbit ventricular myocytes: disruption by hypochlorous acid and restoration by dithiothreitol. Circ. Res. 69: 1132-1138.
Endoh, M. 2006. Signal transduction and Ca2+ signaling in intact myocardium. J. Pharmacol. Sci. 100: 525-537.
Fein, F. S., Kornstein, L. B., Strobeck, J. E., Capasso, J. M., and Sonnenblick, E. H. 1980. Altered myocardial mechanics in diabetic rats. Circ. Res. 47:922-933.
Feldman, A. M. 1993. Classification of positive inotropic agents. J. Am. Coll. Cardiol. 22:1223-1227.
Gao, T., Yatani, A., Dell’Acqua, M. L., Sako, H., Green, S. A., Dascal, N., Scott, J. D., and Hosey, M. M. 1997. AMP-dependent regulation of cardiac L-type Ca2+ channels requires membrane targeting of PKA and phosphorylation of channel subunits. Neuron 19:185-196.
Gocmen, C., Secilmis, A., Kumcu, E. K., Ertug, P. U., Onder, S., Dikmen, A., and Baysal, F. 2000. Effects of vitamin E and sodium selenate on neurogenic and endothelial relaxation of corpus cavernosum in the diabetic mouse. Eur. J. Pharmacol. 398:93-98.
Gopalakrishna, R., and Jaken, S. 2000. Protein kinase C signaling and oxidative stress. Free Radic. Biol. Med. 28:1349-1361.
Hammond, H. K., Roth, D. A., McKirnan, M. D., and Ping, P. 1993. Regional myocardial down-regulation of the inhibitory guanosine triphosphate-binding protein (Gi alpha 2) and beta-adrenergic receptors in a porcine model of chronic episodic myocardial ischemia. J. Clin. Invest. 92:2644-2652.
Handel, M. L., Watts, C. K. W., DeFazio, A., and Grupp, G. 1995. Inhibition of AP-1 binding and transcription by gold and selenium involving conserved cysteine residues in Jun and Fos. Proc. Natl. Acad. Sci. USA 92:4497-4501.
Hartzell, H. C. 1988. Regulation of cardiac ion channels by catecholamines, acetylcholine and second messenger systems. Prog. Biophys. Mol. Biol. 52:165-247.
Hausdorff, W. P., Hnatowich, M., O’Dowd, B. F., Caron, M. G., and Lefkowitz, R. J. 1990. A mutation of the beta 2-adrenergic receptor impairs agonist activation of adenylyl cyclase with-out affecting high affinity agonist binding. Distinct molecular determinants of the receptor are involved in physical coupling to and functional activation of Gs. J. Biol. Chem. 265:1388-1393.
Homcy, C. J., Vatner, S. F., and Vatner, D. E. 1991. Beta-adrenergic receptor regulation in the heart in pathophysiologic states: abnormal adrenergic responsiveness in cardiac disease. Annu. Rev. Physiol. 53:137-159.
Hool, L. C., Middleton, L. M., and Harvey, R. D. 1998. Genistein increases the sensitivity of cardiac ion channels to β-adrenergic receptor stimulation. Circ. Res. 83:33-42.
Iaccarino, G., Lefkowitz, R. J., and Koch, W. J. 1999. Myocardial G protein-coupled receptor kinases: implications for heart failure therapy. Proc. Assoc. Am. Physicians 111:399-405.
Kaul, N., Siveski-Iliskovic, N., Hill, M., Slezak, J., and Singal, P. K. 1993. Free radicals and the heart. J. Pharmacol. Toxicol. Methods 30:55-67.
Kaura, D., Takeda, N., Sethi, R., Wang, X., Nagano, M., and Dhalla, N. S. 1996. Beta-adrenoceptor mediated signal transduction in congestive heart failure in cardiomyopathic (UM-X7.1) ham-sters. Mol. Cell. Biochem. 157:191-196.
Kim, I. Y., and Stadtman, T. C. 1997. Inhibition of NF-κB DNA binding and nitric oxide induction in human T cells and lung adenocarcinoma cells by selenite treatment. Proc. Natl. Acad. Sci. USA 94: 12904-12907.
Koller, L. D., and Exon, J. H. 1986. The two faces of selenium—deficiency and toxicity—-are similar in animals and man. Can. J. Vet. Res. 50:297-306.
Lands, A. M., Arnold, A., McAuliff, J. P., Luduena, F. P., and Brown, T. G., Jr. 1967. Differentiation of receptor systems activated by sympathomimetic amines. Nature 214:597-598.
Le, C. T., Hollaar, L., Van der Valk, E. J., Franken, N. A., Van Ravels, F. J., Wondergem, J., and Van der Laarse, A. 1995. Protection of myocytes against free radical-induced damage by accelerated turnover of the glutathione redox cycle. Eur. Heart J. 16:553-562.
Li, G. S., Wang, F., Kang, D. R., and Li, C. 1985. Keshan disease: an endemic cardiomyopathy in China. Hum. Pathol. 16:602-609.
Li, S., Li, X., and Rozanski, G. J. 2003. Regulation of glutathione in cardiac myocytes. J. Mol. Cell. Cardiol. 35:1145-1152.
Lin-Shiau, S. Y., Liu, S. H., and Fu, W. M. 1989. Studies on the contracture of the mouse diaphragm induced by sodium selenite. Eur. J. Pharmacol. 167:137-146.
Marks, A. R. 2001. Ryanodine receptors/calcium release channels in heart failure and sudden car-diac death. J. Mol. Cell. Cardiol. 33:615-624.
Mohamed, A. K., Bierhaus, A., Schiekofer, S., Tritschler, H., Ziegler, R., and Nawroth, P. P. 1999. The role of oxidative stress and NF-κB activation in late diabetic complications. Biofactors 10: 157-167.
Nishizawa, T., Iwase, M., Kanazawa, H., Ichihara, S., Ichihara, G., Nagata, K., Obata, K., Kitaichi, K., Yokoi, T., Watanabe, M., Tsunematsu, T., Ishikawa, Y., Murohara, T., and Yokota, M. 2004. Serial alterations of beta-adrenergic signaling in dilated cardiomyopathic hamsters: possible role of myocardial oxidative stress. Circ. J. 68:1051-1060.
Oudit, G. Y., Kassiri, Z., Sah, R., Ramirez, R. J., Zobel, C., and Backx, P. H. 2001. The molecu-lar physiology of the cardiac transient outward potassium current (Ito ) in normal and diseased myocardium. J. Mol. Cell. Cardiol. 33:851-872.
Overcast, J. D., Ensley, A. E., Buccafusco, C. J., Cundy, C., Broadnax, R. A., He, S., Yoganathan, A. P., Pollock, S. H., Hartley, C. J., and May, S. W. 2001. Evaluation of cardiovascular parameters of a selenium-based antihypertensive using pulsed Doppler ultrasound. J. Cardiovasc. Pharmacol. 38: 337-346.
Persad, S., Takeda, S., Panagia, V., and Dhalla, N. S. 1997. B-adrenoceptor-linked signal transduc-tion in ischemic-reperfused heart and scavenging of oxyradicals. J. Mol. Cell. Cardiol. 29:545-558.
Pogwizd, S. M., Schlotthauer, K., Li, L., Yuan, W., and Bers, D. M. 2001. Arrhythmogenesis and contractile dysfunction in heart failure: Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness. Circ. Res. 88:1159-1167.
Poltronieri, R., Cevese, A., and Sbartani, A. 1992. Protective effect of selenium in cardiac ischemia and reperfusion. Cardioscience 3:155-160.
Puceat, M., Bony, C., Jaconi, M., and Vassort, G. 1998. Specific activation of adenylyl cyclase V by a purinergic agonist. FEBS Lett. 431:189-194.
Quin, F., Yan, C., Patel, R., Liu, W., and Dong, E. 2006. Vitamin C and E attenuate apoptosis, β-adrenergic receptor desensitization, and sarcoplasmic reticular Ca2+ ATPase downregulation after myocardial infarction. Free Radic. Biol. Med. 40:1827-1842.
Rozanski, G. J., Xu, Z., Zhang, K., and Patel, K. P. 1998. Altered K+ current of ventricular myocytes in rats with chronic myocardial infarction. Am. J. Physiol. 274 (1 Pt 2):H259-H265.
Rozec, B., and Gauthier, C. 2006. B3 -adrenoceptors in the cardiovascular system: putative roles in human pathologies. Pharmacol. Ther. 111:652-673.
Salonen, J. T., Salonen, R., Penttila, I., Herranen, J., Jauhiainen, M., Kantola, S., Lappetelainen, R., Maenpaa, P., Alfthan, G., and Puska, P. 1985. Serum fatty acids, apolipoproteins, selenium and vitamin antioxidants and the risk of death from coronary artery disease. Am. J. Cardiol. 56:226-231.
Sayar, K., Ugur, M., Gurdal, H., Onaran, O., Hotomaroglu, O., and Turan, B. 2000. Dietary selenium and vitamin E intakes alter β-adrenergic response of L-type Ca-current and β-adrenoceptor-adenylate cyclase coupling in rat heart. J. Nutr. 130:733-740.
Schieke, S. M., Briviba, K., Klotz, L. O., and Sies, H. 1999. Activation of mitogen-activated protein kinases elicited by peroxynitrite: attenuation by selenite supplementation. FEBS Lett. 448:301-303.
Schulz, R., Rassaf, T., Massion, P. B., Kelm, M., and Balligand, J. L. 2006. Recent advances in the understanding of the role of nitric oxide in cardiovascular homeostasis. Pharmacol. Ther. 108:225-256.
Sims, C., and Harvey, R. D. 2004. Redox modulation of basal and beta-adrenergically stimulated cardiac L-type Ca2+ channel activity by phenylarsine oxide. Br. J. Pharmacol. 142:797-807.
Stapleton, S. R., Garlock, G., Foellmi-Adam, L., and Kletzien, R. F. 1997. Selenium: potent stim-ulator of tyrosyl phosphorylation and activator of MAP kinase. Biochim. Biophys. Acta 1355: 259-269.
Stiles, G. L., and Lefkowitz, R. J. 1984. Cardiac adrenergic receptors. Annu. Rev. Med. 35:149-164.
Strasser, R. H., Krimmer, J., Braun-Dullaeus, R., Marquetant, R., and Kubler, W. 1990. Dual sen-sitization of the adrenergic system in early myocardial ischemia: independent regulation of the beta-adrenergic receptors and the adenylyl cyclase. J. Mol. Cell. Cardiol. 22:1405-1423.
Sun, Y., and Oberley, L. W. 1996. Redox regulation of transcriptional activators. Free Radic. Biol. Med. 21:335-348.
Tatsumi, T., and Fliss, H. 1994. Hypochlorous acid mobilizes intracellular zinc in isolated rat heart myocytes. J. Mol. Cell. Cardiol. 26:471-479.
Turan, B., Desilets, M., Acan, L. N., Hotomaroglu, O., Vannier, C., and Vassort, G. 1996. Oxidative effects of selenite on rat ventricular contractility and Ca movements. Cardiovasc. Res. 32:351-361.
Turan, B., Fliss, H., and Desilets, M. 1997. Oxidants increase intracellular free Zn2+ concentration in rabbit ventricular myocytes. Am. J. Physiol. Heart Circ. Physiol. 272: H2095-H2106.
Turan, B., Hotomaroglu, O., Kilic, M., and Demirel-Yilmaz, E. 1999. Cardiac dysfunction induced by low and high diet antioxidant levels. Comparing selenium and vitamin E in rats. Regul. Pharmacol. Toxicol. 29:142-150.
Turan, B., Saini, H. K., Zhang, M., Prajapati, D., Elimban, V., and Dhalla, N. S. 2005. Selenium improves cardiac function by attenuating the activation of NF-κB due to ischemia-reperfusion injury. Antioxid. Redox Signal. 7:1388-1397.
Ugur, M., and Turan, B. 2001. Adenosine triphosphate alters the selenite-induced contracture and negative inotropic effect on cardiac muscle contractions. Biol. Trace Elem. Res. 79:235-245.
Ugur, M., Ayaz, M., Ozdemir, S., and Turan, B. 2002. Toxic concentrations of selenite shortens repolarization phase of action potential in rat papillary muscle. Biol. Trace Elem. Res. 89:227-238.
Valen, G., Yan, Z. Q., and Hansson, G. K. 2001. Nuclear factor kappa-B and the heart. J. Am. Coll. Cardiol. 38:307-314.
Webb, T. E., Boluyt, M. O., and Barnard, E. A. 1996. Molecular biology of P2Y purinoceptors: expression in rat heart. J. Auton. Pharmacol. 16:303-307.
Wehrens, X. H., and Marks, A. R. 2003. Altered function and regulation of cardiac ryanodine receptors in cardiac disease. Trends Biochem. Sci. 28:671-678.
Wold, L. E., Ceylan-Isik, A. F., and Ren, J. 2005. Oxidative stress and stress signaling: menace of diabetic cardiomyopathy. Acta Pharmacol. Sin. 26:908-917.
Wold, L. E., Ceylan-Isik, A. F., Fang, C. X., Yang, X., Li, S. Y., Sreejayan, N., Privratsky, J. R., and Ren, J. 2006. Metallothionein alleviates cardiac dysfunction in streptozotocin-induced diabetes: Role of Ca2+ cycling proteins, NADPH oxidase, poly(ADP-ribose) polymerase and myosin heavy chain isozyme. Free Radic. Biol. Med. 40:1419-1429.
Xu, Z., Patel, K. P., Lou, M. F., and Rozanski, G. J. 2002. Up-regulation of K+ channels in diabetic rat ventricular myocytes by insulin and glutathione. Cardiovasc. Res. 53:80-88.
Yaras, N., Ozdemir, S., Ugur, M., Puralı, N., Gurdal, H., Lacampagne, A., Vassort, G., and Turan, B. 2005. Effect of diabetes on ryanodine receptor Ca release channel (RyR2) and Ca2+ homeostasis in rat heart. Diabetes 54:3082-3088.
Ye, G., Metreveli, N. S., Ren, J., and Epstein, P. N. 2003. Metallothionein prevents diabetes-induced deficits in cardiomyocytes by inhibiting reactive oxygen species production. Diabetes 52:777-783.
Zhang, M., Xu, Y. J., Saini, H. K., Turan, B., Liu, P. P., and Dhalla, N. S. 2005. TNF-alpha as a po-tential mediator of cardiac dysfunction due to intracellular Ca2+ -overload. Biochem. Biophys. Res. Commun. 327:57-63.
Zhou, Y. Y., Yao, J. A., and Tsen, G. N. 1997. Role of tyrosine kinase activity in cardiac slow delayed rectifier channel modulation by cell swelling. Pfl ügers Arch. 433:750-757.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2008 Springer Science+Business Media, LLC
About this chapter
Cite this chapter
Turan, B. (2008). Relationship Between Redox Regulation and β-Adrenergic Responses in the Heart. In: Srivastava, A.K., Anand-Srivastava, M.B. (eds) Signal Transduction in the Cardiovascular System in Health and Disease. Advances in Biochemistry in Health and Disease, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-09552-3_8
Download citation
DOI: https://doi.org/10.1007/978-0-387-09552-3_8
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-09551-6
Online ISBN: 978-0-387-09552-3
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)