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European Journal of Heart Failure 2002 4(3):249-254; doi:10.1016/S1388-9842(02)00016-8
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© 2002 European Society of Cardiology

Hypertrophic responsiveness of cardiomyocytes to {alpha}- or β-adrenoceptor stimulation requires sodium-proton-exchanger-1 (NHE-1) activation but not cellular alkalization

Matthias Schäfer, Claudia Schäfer, Hans Michael Piper and Klaus-Dieter Schlüter*

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

* Corresponding author. Tel.: +49-641-99-47-212; fax: +49-641-99-47-239. E-mail address: klaus-dieter.schlueter{at}physiologie.med.uni-giessen.de


  Abstract

The influence of the sodium-proton-exchanger-1 (NHE-1) inhibitor HOE694 on {alpha}- or β-adrenoceptor mediated stimulation of protein synthesis was investigated in cultured ventricular cardiomyocytes from adult rat pre-treated with fetal calf serum to induce hypertrophic responsiveness to β-adrenoceptor stimulation. Stimulation of {alpha}-adrenoceptors with phenylephrine (10 µM) in bicarbonate-free medium caused cellular alkalization ({Delta}pHi: +0.17±0.02, n=5, P<0.05). HOE694, an NHE-1 inhibitor, completely abolished this effect. [14C]phenylalanine incorporation into cellular protein mass increased in the presence of phenylephrine by 23±8%, and this effect was also abolished in the presence of HOE694. HOE694 (1 µM) neither influenced basal protein synthesis nor interfered with {alpha}-adrenoceptor mediated activation of ERK2. Phorbol myristate acetate, a direct stimulator of protein kinase C, mimicked the effect of {alpha}-adrenoceptor stimulation in regard to protein synthesis, but did not lead to cellular alkalization. Protein synthesis increased in the presence of isoprenaline, a β-adrenoceptor agonist also. Again, HOE694 attenuated the stimulation of protein synthesis although isoprenaline did not cause cellular alkalization. In conclusion, the growth response to different hypertrophic stimuli, namely {alpha}- or β-adrenoceptor stimulation, is attenuated in the presence of the NHE-1 inhibitor HOE694 and this inhibition is independent from cellular alkalization.

Key Words: Myocardial hypertrophy • Cellular alkalization • Protein kinase C

Received March 1, 2001; Revised September 4, 2001; Accepted December 1, 2001


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