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EL PAPEL DEL RECEPTOR Β3 ADRENERGICO EN LA FISIOPATOLOGIA DE LA INSUFICIENCIA CARDIACA

(especial para SIIC © Derechos reservados)
El receptor adrenérgico β3 aparenta ser el responsable del efecto inotrópico negativo en los ventrículos de pacientes con insuficiencia cardíaca. Este efecto a largo plazo podría empeorar la disfunción miocárdica.
moniotte9.jpg Autor:
Moniotte, stephane
Columnista Experto de SIIC

Institución:
Department of Cardiology The Children's Hospital Boston, MA, USA


Artículos publicados por Moniotte, stephane
Recepción del artículo
12 de Mayo, 2004
Aprobación
24 de Agosto, 2004
Primera edición
13 de Abril, 2005
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La identificación del gen que codifica el receptor adrenérgico β3 ayudó a interpretar los resultados de experimentos farmacológicos en los que se identificaron efectos atípicos de las catecolaminas diferentes de los observados luego de la activación de los receptores adrenérgicos β1 y β2. En los roedores, el receptor adrenérgico β3 se expresa en el tejido adiposo general y en la grasa parda. El tratamiento de estos animales con agonistas del receptor adrenérgico β3 induce la pérdida de peso secundaria a la estimulación de la lipólisis en ambos tejidos. Sin embargo, el escaso efecto lipolítico sobre el tejido adiposo humano y el descubrimiento reciente de los receptores adrenérgicos β3 en el corazón generan nuevas preguntas acerca del uso de estos agonistas en el hombre. En el ventrículo de los seres humanos, estos agonistas desencadenan un efecto inotrópico negativo. Como este efecto se conserva en el corazón con insuficiencia cardíaca podría explicar el papel que desempeña el aumento del estímulo adrenérgico asociado con la insuficiencia cardíaca, como también el tratamiento de esta condición con bloqueantes de los receptores betadrenérgicos. Esta revisión resume los efectos y la justificación del bloqueo betadrenérgico en la insuficiencia cardíaca crónica y principalmente trata de responder a la pregunta acerca del uso potencial de antagonistas de los receptores β3 en el tratamiento de esta insuficiencia.

Palabras clave
Receptores, adrenérgico, catecolaminas, contractilidad, insuficiencia cardíaca


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Abstract
The characterization of the gene encoding the β3-adrenoceptor helped to interpret the results of pharmacological experiments on atypical effects of catecholamines distinct from the classical activation of β1 and β2 adrenoceptors. In rodents, the β3 adrenoceptor is abundantly expressed in white adipose tissue as well as in brown adipose tissue. Treatment of rodents with β3 adrenoceptor agonists induces a weight loss related to the stimulation of lipolysis in these two tissues. However, their poor lipolytic effect in human adipose tissue and the recent discovery of functional β3 adrenoceptors in the human heart raise new questions on the use of agonists in man. In the human ventricle, these agonists induce a negative inotropic effect. As this effect is conserved in the failing heart, it could shed a new light on the pathogenic role of the hyperadrenergism associated with cardiac failure, as well as on its treatment with beta-adrenoceptor blockers. This review summarizes the rationale and effects of beta-adrenergic blockade in chronic heart failure and specifically addresses the question of the potential use of β3-adrenoceptor antagonists in the treatment of heart failure and other pathophysiological conditions associated with a decreased cardiac contractility.

Key words
Receptors, adrenergic, catecholamines, contractility, heart failure, sepsis


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Especialidades
Principal: Cardiología
Relacionadas: Farmacología, Geriatría, Medicina Farmacéutica, Medicina Interna



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Bibliografía del artículo
  1. Thomas JA, Marks BH. Plasma norepinephrine in congestive heart failure. Am J Cardiol 1978; 41(2):233-243.
  2. Cohn JN, Levine TB, Olivari MT et al. T. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med 1984; 311(13):819-823.
  3. Gaffney TE, Braunwald E. Importance of adrenergic nervous systme in the support of circulatory function in patients with congestive heart failure. Am J Med 1963; 34:320-324.
  4. Packer M. Pathophysiology of chronic heart failure. Lancet 1992; 340(8811):88-92.
  5. Gauthier C, Tavernier G, Charpentier F et al. Functional beta3-adrenoceptor in the human heart. J Clin Invest 1996; 98(2):556-562.
  6. Gauthier C, Leblais V, Kobzik L et al. The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle. J Clin Invest 1998; 102(7):1377-1384.
  7. Swedberg K, Viquerat C, Rouleau JL et al.. Comparison of myocardial catecholamine balance in chronic congestive heart failure and in angina pectoris without failure. Am J Cardiol 1984; 54(7):783-786.
  8. Hasking GJ, Esler MD, Jennings GL et al. Norepinephrine spillover to plasma in patients with congestive heart failure: evidence of increased overall and cardiorenal sympathetic nervous activity. Circulation 1986; 73(4):615-621.
  9. Haber HL, Simek CL, Gimple LW et al. Why do patients with congestive heart failure tolerate the initiation of beta-blocker therapy Circulation 1993; 88(4 Pt 1):1610-1619.
  10. Goldsmith SR, Francis GS, Cohn JN. Norepinephrine infusions in congestive heart failure. Am J Cardiol 1985; 56(12):802-804.
  11. Bristow MR, Minobe W, Rasmussen R et al. Beta-adrenergic neuroeffector abnormalities in the failing human heart are produced by local rather than systemic mechanisms. J Clin Invest 1992; 89(3):803-815.
  12. Kaye DM, Lefkovits J, Jennings GL et al. Adverse consequences of high sympathetic nervous activity in the failing human heart. J Am Coll Cardiol 1995; 26(5):1257-1263.
  13. Bristow MR, Ginsburg R, Umans V et al. Beta 1- and beta 2-adrenergic-receptor subpopulations in nonfailing and failing human ventricular myocardium: coupling of both receptor subtypes to muscle contraction and selective beta 1-receptor down-regulation in heart failure. Circ Res 1986; 59(3):297-309.
  14. Brodde OE, Schuler S, Kretsch R et al. Regional distribution of beta-adrenoceptors in the human heart: coexistence of functional beta 1- and beta 2-adrenoceptors in both atria and ventricles in severe congestive cardiomyopathy. J Cardiovasc Pharmacol 1986; 8(6):1235-1242.
  15. Bristow MR. Changes in myocardial and vascular receptors in heart failure. J Am Coll Cardiol 1993; 22(4 Suppl A):61A-71A.
  16. Mann DL, Kent RL, Parsons B et al. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation 1992; 85(2):790-804.
  17. Engelhardt S, Hein L, Wiesmann F et al. Progressive hypertrophy and heart failure in beta1-adrenergic receptor transgenic mice. Proc Natl Acad Sci USA 1999; 96(12):7059-7064.
  18. Iwase M, Bishop SP, Uechi M et al. Adverse effects of chronic endogenous sympathetic drive induced by cardiac GS alpha overexpression. Circ Res 1996; 78(4):517-524.
  19. D’Angelo DD, Sakata Y, Lorenz JN et al. Transgenic Galphaq overexpression induces cardiac contractile failure in mice. Proc Natl Acad Sci U S A 1997; 94(15):8121-8126.
  20. Communal C, Singh K, Pimentel DR et al. Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway. Circulation 1998; 98(13):1329-1334.
  21. Communal C, Singh K, Sawyer DB et al. Opposing effects of beta(1)- and beta(2)-adrenergic receptors on cardiac myocyte apoptosis : role of a pertussis toxin-sensitive G protein. Circulation 1999; 100(22):2210-2212.
  22. Chesley A, Lundberg MS, Asai T et al. The Beta2-adrenergic receptor delivers an antiapoptotic signal to cardiac myocytes through G(i)-dependent coupling to phosphatidylinositol 3'-kinase. Circ Res 2000; 87(12):1172-1179.
  23. Liggett SB, Tepe NM, Lorenz JN et al. Early and delayed consequences of beta-2 adrenergic receptor overexpression in mouse hearts. Circulation 2000; 101:1707-1714.
  24. Milano CA, Dolber PC, Rockman HA et al. Myocardial expression of a constitutively active alpha 1B-adrenergic receptor in transgenic mice induces cardiac hypertrophy. Proc Natl Acad Sci U S A 1994; 91(21):10109-10113.
  25. Ungerer M, Bohm M, Elce JS et al. Altered expression of beta-adrenergic receptor kinase and beta 1- adrenergic receptors in the failing human heart. Circulation 1993; 87(2):454-463.
  26. Tan LB, Benjamin IJ, Clark WA. Beta Adrenergic receptor desensitisation may serve a cardioprotective role. Cardiovasc Res 1992; 26(6):608-614.
  27. Bristow MR. The adrenergic nervous system in heart failure. N Engl J Med 1984; 311(13):850-851.
  28. Gauthier C, Tavernier G, Charpentier F et al. Functional beta3-adrenoceptor in the human heart. J Clin Invest 1996; 98(2):556-562.
  29. Gauthier C, Leblais V, Kobzik L et al. The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle. J Clin Invest 1998; 102(7):1377-1384.
  30. Berkowitz DE, Nardone NA, Smiley RM et al. Distribution of beta 3-adrenoceptor mRNA in human tissues. Eur J Pharmacol 1995; 289(2):223-228
  31. Krief S, Lonnqvist F, Raimbault S et al. Tissue distribution of beta 3-adrenergic receptor mRNA in man. J Clin Invest 1993; 91(1):344-349.
  32. Moniotte S, Kobzik L, Feron O et al. The altered response to adrenergic stimulation in human failing hearts is associated with an upregulation of the 3 adrenoceptor and its coupled Gi-protein. Circulation 2001; 103 :1649-1655 .
  33. Begin-Heick N. Beta 3-adrenergic activation of adenylyl cyclase in mouse white adipocytes: modulation by GTP and effect of obesity. J Cell Biochem 1995; 58(4):464-473.
  34. Chaudhry A, Granneman JG. Influence of cell type upon the desensitization of the beta 3- adrenergic receptor. J Pharmacol Exp Ther 1994; 271(3):1253-1258.
  35. Balligand JL, Kelly RA, Marsden PA et al. Control of cardiac muscle cell function by an endogenous nitric oxide signaling system. Proc Natl Acad Sci U S A 1993; 90(1):347-351.
  36. Varghese PG, Ricker KM, Georgakopoulos D et al. Mice with homozygous beta 3 adrenoceptor deletion mutations do not exhibit nitric oxide inhibition of myocardial contractility. Circulation 100, Suppl I-338, 1772-1772. 1999.
  37. Wahler GM, Dollinger SJ. Nitric oxide donor SIN-1 inhibits mammalian cardiac calcium current through cGMP-dependent protein kinase. Am J Physiol 1995; 268(1 Pt 1):C45-C54.
  38. Mery PF, Lohmann SM, Walter U, et al. Ca2+ current is regulated by cyclic GMP-dependent protein kinase in mammalian cardiac myocytes. Proc Natl Acad Sci U S A 1991; 88(4):1197-1201.
  39. Shah AM, Mebazaa A, Wetzel RC et al. Novel cardiac myofilament desensitizing factor released by endocardial and vascular endothelial cells. Circulation 1994; 89(6):2492-2497.
  40. Mery PF, Pavoine C, Belhassen L et al. Nitric oxide regulates cardiac Ca2+ current. Involvement of cGMP- inhibited and cGMP-stimulated phosphodiesterases through guanylyl cyclase activation. J Biol Chem 1993; 268(35):26286-26295.
  41. Campbell DL, Stamler JS, Strauss HC. Redox modulation of L-type calcium channels in ferret ventricular myocytes. Dual mechanism regulation by nitric oxide and S-nitrosothiols. J Gen Physiol 1996; 108(4):277-293.
  42. Gross WL, Bak MI, Ingwall JS et al. Nitric oxide inhibits creatine kinase and regulates rat heart contractile reserve. Proc Natl Acad Sci U S A 1996; 93(11):5604-5609.
  43. Torres J, Darley-Usmar V, Wilson MT. Inhibition of cytochrome c oxidase in turnover by nitric oxide: mechanism and implications for control of respiration. Biochem J 1995; 312 (Pt 1):169-173.
  44. Massion, PB, Moniotte S, Balligand JL. Nitric oxide: does it play a role in the heart of the critically ill Curr Opin Crit Care 2001; 7(5): 323-336.
  45. Massion PB, Feron O, Dessy Cet al. Nitric oxide and cardiac function: ten years after, and continuing. Circ Res. 2003 Sep 5;93(5):388-98.
  46. Leblais V, Demolombe S, Vallette G et al. Beta3-adrenoceptor control the cystic fibrosis transmembrane conductance regulator through a cAMP/protein kinase A-independent pathway. J Biol Chem 1999; 274(10):6107-6113.
  47. Riordan JR, Rommens JM, Kerem B et al. Identification of the cystic fibrosis gene: cloning and characterization of complementary DNA. Science 1989; 245(4922):1066-1073.
  48. Kathofer S, Zhang W, Karle C et al. Functional Coupling of Human beta 3-Adrenoreceptors to the KvLQT1/MinK Potassium Channel. J Biol Chem 2000; 275(35):26743-26747.
  49. Leblais V, Escande D, Gauthier C. Beta-3 adrenoceptors regulate CFTR conductance through a PTX-sensitive G protein. Circulation 100[18], I-488. 1999.
  50. Bosch RF, Schneck AC, Kiehn J et al. Beta3-Adrenergic regulation of an ion channel in the heart-inhibition of the slow delayed rectifier potassium current I(Ks) in guinea pig ventricular myocytes. Cardiovasc Res. 2002 Dec;56(3):393-403.
  51. Bristow MR. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med 1982; 4(307):205-211.
  52. Brodde OE. Beta 1- and beta 2-adrenoceptors in the human heart: properties, function, and alterations in chronic heart failure. Pharmacol Rev 1991; 43(2):203-242.
  53. Bohm M, Lohse MJ. Quantification of beta-adrenoceptors and beta-adrenoceptor kinase on protein and mRNA levels in heart failure. Eur Heart J 1994; 15 Suppl D:30-34.
  54. Ungerer M, Bohm M, Elce JS et al. Altered expression of beta-adrenergic receptor kinase and beta 1- adrenergic receptors in the failing human heart. Circulation 1993; 87(2):454-463.
  55. Bohm M, Eschenhagen T, Gierschik P, Larisch K, Lensche H, Mende U, Schmitz W, Schnabel P, Scholz H, Steinfath M. Radioimmunochemical quantification of Gi alpha in right and left ventricles from patients with ischaemic and dilated cardiomyopathy and predominant left ventricular failure. J Mol Cell Cardiol 1994; 26(2):133-149.
  56. Feldman AM, Cates AE, Veazey WB, Hershberger RE, Bristow MR, Baughman KL, Baumgartner WA, Van Dop C. Increase of the 40,000-mol wt pertussis toxin substrate (G protein) in the failing human heart. J Clin Invest 1988; 82(1):189-197.
  57. Langin D, Tavernier G, Lafontan M. Regulation of beta 3-adrenoceptor expression in white fat cells. Fundam Clin Pharmacol 1995; 9(2):97-106.
  58. Emorine LJ, Marullo S, Briend-Sutren MM, Patey G, Tate K, Delavier-Klutchko C, Strosberg AD. Molecular characterization of the human beta 3-adrenergic receptor. Science 1989; 245(4922):1118-1121.
  59. Tavernier G, Toumaniantz G, Erfanian M et al. Beta3-Adrenergic stimulation produces a decrease of cardiac contractility ex vivo in mice overexpressing the human beta3-adrenergic receptor. Cardiovasc Res. 2003 Aug 1;59(2):288-96.
  60. Morimoto A, Hasegawa H, Cheng HJ et al. Endogenous beta 3-adrenoceptor activation contributes to left ventricular and cardiomyocyte dysfunction in heart failure. Am J Physiol Heart Circ Physiol. 2004 Feb 12.
  61. Pott C, Brixius K, Bundkirchen A et al. The preferential beta3-adrenoceptor agonist BRL 37344 increases force via beta1-/beta2-adrenoceptors and induces endothelial nitric oxide synthase via beta3-adrenoceptors in human atrial myocardium. Br J Pharmacol. 2003 Feb;138(3):521-9.
  62. Manara L, Badone D, Baroni M et al. Functional identification of rat atypical beta-adrenoceptors by the first beta 3-selective antagonists, aryloxypropanolaminotetralins. Br J Pharmacol 1996; 117(3):435-442.
  63. De Ponti F, Gibelli G, Croci T et al. Functional evidence of atypical beta 3-adrenoceptors in the human colon using the beta 3-selective adrenoceptor antagonist, SR 59230A. Br J Pharmacol 1996; 117(7):1374-1376.
  64. Nisoli E, Tonello C, Landi M et al. Functional studies of the first selective beta 3-adrenergic receptor antagonist SR 59230A in rat brown adipocytes. Mol Pharmacol 1996; 49(1):7-14.
  65. Kaumann AJ, Molenaar P. Differences between the third cardiac beta-adrenoceptor and the colonic beta 3-adrenoceptor in the rat. Br J Pharmacol 1996; 118(8):2085-2098.
  66. Malinowska B, Schlicker E. Further evidence for differences between cardiac atypical beta- adrenoceptors and brown adipose tissue beta3-adrenoceptors in the pithed rat. Br J Pharmacol 1997; 122(7):1307-1314.
  67. Trochu JN, Leblais V, Rautureau Y et al. Beta 3-adrenoceptor stimulation induces vasorelaxation mediated essentially by endothelium-derived nitric oxide in rat thoracic aorta. Br J Pharmacol 1999; 128(1):69-76.
  68. Candelore MR, Deng L, Tota L et al. Potent and selective human beta(3)-adrenergic receptor antagonists. J Pharmacol Exp Ther 1999; 290(2):649-655.

 
 
 
 
 
 
 
 
 
 
 
 
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