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Cardiovascular Research 2002 53(4):879-887; doi:10.1016/S0008-6363(01)00517-X
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Neuropeptide Y modifies the hypertrophic response of adult ventricular cardiomyocytes to norepinephrine

Marat Kanevskij, Gerhild Taimor, Matthias Schäfer, Hans Michael Piper and Klaus-Dieter Schlüter*

Physiologisches Institut, Justus-Liebig-Universität Gießen, Aulweg 129, D-35392 Gießen, Germany

klaus-dieter.schlueter{at}physiologie.med.uni-giessen.de

* Corresponding author. Tel.: +49-641-9947-212; fax: +49-641-9947-239

Objective: The hypertrophic response of adult rat cardiomyocytes to norepinephrine via {alpha}-adrenoceptor stimulation is limited by an inhibitory cross-talk of simultaneously β-adrenoceptor stimulation. On the other hand, neuropeptide Y (NPY), known to be co-secreted with norepinephrine from intramural nerve endings of the heart, exerts an anti-β-adrenergic effect. Therefore, it should be expected that NPY enhances the hypertrophic response to norepinephrine. This hypothesis was addressed in the present study. Methods: Isolated adult ventricular cardiomyocytes from rats were used. As parameters of hypertrophic growth we investigated cell volume, cross-sectional area, protein mass. Protein and RNA synthesis were determined by incorporation of [14C]phenylalanine or [14C]uridine, respectively. Results: Norepinephrine (1 µmol/l) did not significantly increase protein or RNA synthesis. In co-presence of NPY (100 nmol/l), however, norepinephrine increased protein synthesis by 44% and RNA synthesis by 18%. Under the same conditions, NPY enhanced the effect of norepinephrine on cell volume from +6.4 to +18.2%, its effect on cross-sectional area from +16 to +23%, and increased the protein/DNA ratio from 32.5 to 35.6 mg/mg. In parallel, norepinephrine caused a translocation of PKC-{alpha} and PKC-{delta} into the particular fractions and this effect of norepinephrine was also enhanced by co-presence of NPY. In contrast, NPY did not enhance ERK-activation caused by norepinephrine. Conclusion: Our study indicates the anti-β-adrenergic effect of NPY is sufficient to modulate the hypertrophic response of adult ventricular cardiomyocytes to norepinephrine. The results suggest that the hypertrophic effect of norepinephrine via {alpha}-adrenoceptor stimulation can be modulated by co-release of NPY from intramural nerve endings.

KEYWORDS Adrenergic (ant)agonists; Hypertrophy; Myocytes; Neurotransmitters; Signal transduction


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