Different Effects of Prolonged β-adrenergic Stimulation on Heart and Cerebral Artery

Overview

Journal Integr Med Res

Publisher Elsevier

Specialty Rehabilitation Medicine

Date 2017 Jul 1

PMID 28664099

Citations 10

Authors

Eunji Shin

Kyung Soo Ko

Byoung Doo Rhee

Jin Han

Nari Kim

Affiliations

Soon will be listed here.

Abstract

The aim of this review was to understand the effects of β-adrenergic stimulation on oxidative stress, structural remodeling, and functional alterations in the heart and cerebral artery. Diverse stimuli activate the sympathetic nervous system, leading to increased levels of catecholamines. Long-term overstimulation of the β-adrenergic receptor (βAR) in response to catecholamines causes cardiovascular diseases, including cardiac hypertrophy, stroke, coronary artery disease, and heart failure. Although catecholamines have identical sites of action in the heart and cerebral artery, the structural and functional modifications differentially activate intracellular signaling cascades. βAR-stimulation can increase oxidative stress in the heart and cerebral artery, but has also been shown to induce different cytoskeletal and functional modifications by modulating various components of the βAR signal transduction pathways. Stimulation of βAR leads to cardiac dysfunction due to an overload of intracellular Ca in cardiomyocytes. However, this stimulation induces vascular dysfunction through disruption of actin cytoskeleton in vascular smooth muscle cells. Many studies have shown that excessive concentrations of catecholamines during stressful conditions can produce coronary spasms or arrhythmias by inducing Ca-handling abnormalities and impairing energy production in mitochondria, In this article, we highlight the different fates caused by excessive oxidative stress and disruptions in the cytoskeletal proteome network in the heart and the cerebral artery in responsed to prolonged βAR-stimulation.

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References

Neumann S, Jennings J, Muldoon M, Manuck S . White-coat hypertension and autonomic nervous system dysregulation. Am J Hypertens. 2005; 18(5 Pt 1):584-8. DOI: 10.1016/j.amjhyper.2004.11.034. View

Dragunow M, Preston K . The role of inducible transcription factors in apoptotic nerve cell death. Brain Res Brain Res Rev. 1995; 21(1):1-28. DOI: 10.1016/0165-0173(95)00003-l. View

Chesley A, Lundberg M, Asai T, Xiao R, Ohtani S, Lakatta E . The beta(2)-adrenergic receptor delivers an antiapoptotic signal to cardiac myocytes through G(i)-dependent coupling to phosphatidylinositol 3'-kinase. Circ Res. 2000; 87(12):1172-9. DOI: 10.1161/01.res.87.12.1172. View

Errami M, Galindo C, Tassa A, Dimaio J, Hill J, Garner H . Doxycycline attenuates isoproterenol- and transverse aortic banding-induced cardiac hypertrophy in mice. J Pharmacol Exp Ther. 2007; 324(3):1196-203. DOI: 10.1124/jpet.107.133975. View

Davel A, Fukuda L, De Sa L, Munhoz C, Scavone C, Sanz-Rosa D . Effects of isoproterenol treatment for 7 days on inflammatory mediators in the rat aorta. Am J Physiol Heart Circ Physiol. 2008; 295(1):H211-9. DOI: 10.1152/ajpheart.00581.2007. View

Keles M, Bayir Y, Suleyman H, Halici Z . Investigation of effects of Lacidipine, Ramipril and Valsartan on DNA damage and oxidative stress occurred in acute and chronic periods following isoproterenol-induced myocardial infarct in rats. Mol Cell Biochem. 2009; 328(1-2):109-17. DOI: 10.1007/s11010-009-0080-y. View

Lechat P, Packer M, Chalon S, Cucherat M, Arab T, Boissel J . Clinical effects of beta-adrenergic blockade in chronic heart failure: a meta-analysis of double-blind, placebo-controlled, randomized trials. Circulation. 1998; 98(12):1184-91. DOI: 10.1161/01.cir.98.12.1184. View

Iaccarino G, Tomhave E, Lefkowitz R, Koch W . Reciprocal in vivo regulation of myocardial G protein-coupled receptor kinase expression by beta-adrenergic receptor stimulation and blockade. Circulation. 1998; 98(17):1783-9. DOI: 10.1161/01.cir.98.17.1783. View

Kim N, Chung J, Kim E, Han J . Changes in the Ca2+-activated K+ channels of the coronary artery during left ventricular hypertrophy. Circ Res. 2003; 93(6):541-7. DOI: 10.1161/01.RES.0000090087.66390.F2. View

10.

Krown K, Page M, Nguyen C, Zechner D, Gutierrez V, Comstock K . Tumor necrosis factor alpha-induced apoptosis in cardiac myocytes. Involvement of the sphingolipid signaling cascade in cardiac cell death. J Clin Invest. 1996; 98(12):2854-65. PMC: 507753. DOI: 10.1172/JCI119114. View

11.

Hanada K, Asari K, Saito M, Kawana J, Mita M, Ogata H . Comparison of pharmacodynamics between carvedilol and metoprolol in rats with isoproterenol-induced cardiac hypertrophy: effects of carvedilol enantiomers. Eur J Pharmacol. 2008; 589(1-3):194-200. DOI: 10.1016/j.ejphar.2008.04.055. View

12.

Yasuhara S, Zhu Y, Matsui T, Tipirneni N, Yasuhara Y, Kaneki M . Comparison of comet assay, electron microscopy, and flow cytometry for detection of apoptosis. J Histochem Cytochem. 2003; 51(7):873-85. DOI: 10.1177/002215540305100703. View

13.

Remiao F, Carmo H, Carvalho F, Bastos M . Inhibition of glutathione reductase by isoproterenol oxidation products. J Enzyme Inhib. 2000; 15(1):47-61. View

14.

Corbi G, Conti V, Russomanno G, Longobardi G, Furgi G, Filippelli A . Adrenergic signaling and oxidative stress: a role for sirtuins?. Front Physiol. 2013; 4:324. PMC: 3820966. DOI: 10.3389/fphys.2013.00324. View

15.

Kang Y . Cardiac hypertrophy: a risk factor for QT-prolongation and cardiac sudden death. Toxicol Pathol. 2006; 34(1):58-66. DOI: 10.1080/01926230500419421. View

16.

Levy D, Garrison R, Savage D, Kannel W, CASTELLI W . Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990; 322(22):1561-6. DOI: 10.1056/NEJM199005313222203. View

17.

Tse J, Powell J, Baste C, PRIEST R, Kuo J . Isoproterenol-induced cardiac hypertrophy: modifications in characteristics of beta-adrenergic receptor, adenylate cyclase, and ventricular contraction. Endocrinology. 1979; 105(1):246-55. DOI: 10.1210/endo-105-1-246. View

18.

Kureishi Y, Kobayashi S, Amano M, Kimura K, Kanaide H, Nakano T . Rho-associated kinase directly induces smooth muscle contraction through myosin light chain phosphorylation. J Biol Chem. 1997; 272(19):12257-60. DOI: 10.1074/jbc.272.19.12257. View

19.

Rodrigo C, Weerasinghe S, Jeevagan V, Rajapakse S, Constantine G . Addressing the relationship between cardiac hypertrophy and ischaemic stroke: an observational study. Int Arch Med. 2012; 5(1):32. PMC: 3549944. DOI: 10.1186/1755-7682-5-32. View

20.

Zheng M, Zhu W, Han Q, Xiao R . Emerging concepts and therapeutic implications of beta-adrenergic receptor subtype signaling. Pharmacol Ther. 2005; 108(3):257-68. DOI: 10.1016/j.pharmthera.2005.04.006. View