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Am J Physiol Heart Circ Physiol 279: H2502-H2508, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2502-H2508, November 2000

Altered beta -adrenergic signal transduction in nonfailing hypertrophied myocytes from Dahl salt-sensitive rats

Kohzo Nagata3, Catherine Communal2, Chee C. Lim1, Mohit Jain1, Thomas M. Suter4, Franz R. Eberli4, Naoya Satoh5, Wilson S. Colucci2, Carl S. Apstein1, and Ronglih Liao1

1 Cardiac Muscle Research Laboratory and 2 Myocardial Biology Unit, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118; 3 First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya 466-8550, Japan; 4 Swiss Cardiovascular Center, University Hospital, 3010 Bern, Switzerland; and 5 Mitsubishi Chemical Corporation Research Center, Aoba-ku, Yokohama 227, Japan

Desensitization of the beta -adrenergic receptor (beta -AR) response is well documented in hypertrophied hearts. We investigated whether beta -AR desensitization is also present at the cellular level in hypertrophied myocardium, as well as the physiological role of inhibitory G (Gi) proteins and the L-type Ca2+ channel in mediating beta -AR desensitization. Left ventricular (LV) myocytes were isolated from hypertrophied hearts of hypertensive Dahl salt-sensitive (DS) rats and nonhypertrophied hearts of normotensive salt-resistant (DR) rats. Cells were paced at a rate of 300 beats/min at 37°C, and myocyte contractility and intracellular Ca2+ concentration ([Ca2+]i) were simultaneously measured. In response to increasing concentrations of isoproterenol, DR myocytes displayed a dose-dependent augmentation of cell shortening and the [Ca2+]i transient amplitude, whereas hypertrophied DS myocytes had a blunted response of both cell shortening and the [Ca2+]i transient amplitude. Interestingly, inhibition of Gi proteins did not restore beta -AR desensitization in DS myocytes. The responses to increases in extracellular Ca2+ and an L-type Ca2+ channel agonist were also similar in both DS and DR myocytes. Isoproterenol-stimulated adenylyl cyclase activity, however, was blunted in hypertrophied myocytes. We concluded that compensated ventricular hypertrophy results in a blunted contractile response to beta -AR stimulation, which is present at the cellular level and independent of alterations in inhibitory G proteins and the L-type Ca2+ channel.

hypertension; hypertrophy; beta -adrenergic desensitization


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