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(Received for publication, January 15, 1997, and in revised form, April 3, 1997)
From the Department of Medicine, University of California, San
Diego, School of Medicine, La Jolla, California 92093 and the
Pressure overload cardiac hypertrophy in the
mouse was achieved following 7 days of transverse aortic constriction.
This was associated with marked
Volume 272, Number 27,
Issue of July 4, 1997
pp. 17223-17229
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
-Adrenergic Receptor Desensitization in Cardiac
Hypertrophy Is Increased -Adrenergic Receptor Kinase
,
Department of Surgery, Duke University,
Durham, North Carolina 27710
-adrenergic receptor (-AR)
desensitization in vivo, as determined by a blunted
inotropic response to dobutamine. Extracts from hypertrophied hearts
had 
3-fold increase in cytosolic and membrane G protein-coupled
receptor kinase (GRK) activity. Incubation with specific monoclonal
antibodies to inhibit different GRK subtypes showed that the increase
in activity could be attributed predominately to the -adrenergic
receptor kinase (ARK). Although overexpression of a ARK inhibitor
in hearts of transgenic mice did not alter the development of cardiac
hypertrophy, the -AR desensitization associated with pressure
overload hypertrophy was prevented. To determine whether the induction
of ARK occurred because of a generalized response to cellular
hypertrophy, ARK activity was measured in transgenic mice homozygous
for oncogenic ras overexpression in the heart. Despite
marked cardiac hypertrophy, no difference in ARK activity was found
in these mice overexpressing oncogenic ras compared with
controls. Taken together, these data suggest that ARK is a central
molecule involved in alterations of -AR signaling in pressure
overload hypertrophy. The mechanism for the increase in ARK activity
appears not to be related to the induction of cellular hypertrophy but
to possibly be related to neurohumoral activation.
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H. A. Rockman, K. R. Chien, D.-J. Choi, G. Iaccarino, J. J. Hunter, J. Ross Jr., R. J. Lefkowitz, and W. J. Koch Expression of a beta -adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice PNAS, June 9, 1998; 95(12): 7000 - 7005. [Abstract] [Full Text] [PDF]
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S. A. Akhter, L. M. Luttrell, H. A. Rockman, G. Iaccarino, R. J. Lefkowitz, and W. J. Koch Targeting the Receptor-Gq Interface to Inhibit in Vivo Pressure Overload Myocardial Hypertrophy Science, April 24, 1998; 280(5363): 574 - 577. [Abstract] [Full Text]
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S. A. Akhter, C. A. Skaer, A. P. Kypson, P. H. McDonald, K. C. Peppel, D. D. Glower, R. J. Lefkowitz, and W. J. Koch Restoration of beta -adrenergic signaling in failing cardiac ventricular myocytes via adenoviral-mediated gene transfer PNAS, October 28, 1997; 94(22): 12100 - 12105. [Abstract] [Full Text] [PDF]
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S. A. Akhter, C. A. Milano, K. F. Shotwell, M.-C. Cho, H. A. Rockman, R. J. Lefkowitz, and W. J. Koch Transgenic Mice with Cardiac Overexpression of alpha 1B-Adrenergic Receptors. IN VIVO alpha 1-ADRENERGIC RECEPTOR-MEDIATED REGULATION OF beta -ADRENERGIC SIGNALING J. Biol. Chem., August 22, 1997; 272(34): 21253 - 21259. [Abstract] [Full Text] [PDF]
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S. V. Naga Prasad, L. S. Barak, A. Rapacciuolo, M. G. Caron, and H. A. Rockman Agonist-dependent Recruitment of Phosphoinositide 3-Kinase to the Membrane by beta -Adrenergic Receptor Kinase 1. A ROLE IN RECEPTOR SEQUESTRATION J. Biol. Chem., May 25, 2001; 276(22): 18953 - 18959. [Abstract] [Full Text] [PDF]
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D. C. White, J. A. Hata, A. S. Shah, D. D. Glower, R. J. Lefkowitz, and W. J. Koch Preservation of myocardial beta -adrenergic receptor signaling delays the development of heart failure after myocardial infarction PNAS, May 9, 2000; 97(10): 5428 - 5433. [Abstract] [Full Text] [PDF]
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V. B. Harding, L. R. Jones, R. J. Lefkowitz, W. J. Koch, and H. A. Rockman Cardiac beta ARK1 inhibition prolongs survival and augments beta blocker therapy in a mouse model of severe heart failure PNAS, May 8, 2001; 98(10): 5809 - 5814. [Abstract] [Full Text] [PDF]
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C. L. Antos, N. Frey, S. O. Marx, S. Reiken, M. Gaburjakova, J. A. Richardson, A. R. Marks, and E. N. Olson Dilated Cardiomyopathy and Sudden Death Resulting From Constitutive Activation of Protein Kinase A Circ. Res., November 23, 2001; 89(11): 997 - 1004. [Abstract] [Full Text] [PDF]
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