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(Hypertension. 1998;32:831-837.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Chamber-Specific Alterations of Norepinephrine Uptake Sites in Cardiac Hypertrophy

Michael Böhm; Maurizio Castellano; Markus Flesch; Christoph Maack; Marianne Moll; Martin Paul; Frank Schiffer; ; Oliver Zolk

From the Klinik III für Innere Medizin der Universität zu Köln, Köln (M.B., M.F., C.M., M.M., F.S., O.Z.), and the Institut für Klinische Pharmakologie und Toxikologie der Freien Universität Berlin, Universitätsklinikum Benjamin Franklin, Berlin (M.P.), Germany; and the Scienze Mediche, Universita degli Studi di Brescia, Italy (M.C.).

Correspondence to Michael Böhm, Klinik III für Innere Medizin der Universität zu Köln, Joseph-Stelzmann-Str. 9, 50924 Köln, Germany.

Abstract—The present study investigated local differences of sympathetic activation and sympathetic neuroeffector defects in nonhypertrophied right and hypertrophied left ventricles in a rat model with renin-induced pressure overload [TG(mREN2)27]. As judged from the depletion of myocardial norepinephrine stores, sympathetic activation was more pronounced in the left than in the right ventricles. In addition, norepinephrine uptake₁ carrier sites were reduced in left but unchanged in right ventricles. Gene expression of the carrier was unchanged in stellate ganglia. An increase of G_i expression and a heterologous adenylyl cyclase desensitization occurred only in the left but not in the right ventricles, whereas a reduction of ß-adrenergic receptors was observed in both chambers. We concluded that general sympathetic activation can lead to ß-adrenoceptor downregulation but that pressure overload further increases sympathetic activation involving norepinephrine uptake mechanisms in the left ventricles, resulting in heterologous ß-adrenergic desensitization.

Key Words: hypertrophy, cardiac • G proteins • adenylyl cyclase • catecholamines

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