Τόμος 7 (1993) – Τεύχος 2 – Άρθρο 3 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 7 (1993) – Issue 2 – Article 3 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

By | | Hans Vetter, Ludwig Neyses, Άρθρο επισκόπησης - Review Article, Ιωάννης Νούσκας - Ioannis Nouskas, Πλήρες Κείμενο στα Αγγλικά - Full Text in English

 

Title Effect of nisoldipine on endothelin-1 and angiotensin II-induced immediate/early gene expression and protein synthesis in adult rat ventricular cardiomyocytes
Authors Ioannis Nouskas, Ludwig Neyses and Hans Vetter

Medical Policlinic, Molecular Cardiology Laboratory, University of Bonn, Federal Republic of Germany (Head: Prof. Dr. med. Hans Vetter)
Citation Nouskas, I., Neyses, L., Vetter, H.: Continuous spinal anesthesia with combination of local anesthetics: Effect of nisoldipine on endothelin-1 and angiotensin II-induced immediate/early gene expression and protein synthesis in adult rat ventricular cardiomyocytes, Epitheorese Klin. Farmakol. Farmakokinet. 7(2): 79-87 (1993)
Publication Date Received for publication: 20 May 1993

 Accepted for publication: 20 June 1993
Full Text Language English
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Keywords Cardiac hypertrophy, Ca antagonists, transcription factors, growth induction.
Other Terms review article
Summary A question of considerable clinical significance is the therapeutic approach to reducing hypertensive left ventricular hypertrophy, as well as the nature of the molecular signals that initiate and maintain cardiac hypertrophy and its regression. We therefore investigated the direct effect of the novel Ca²+ blocker nisoldipine (N) in inhibiting growth-related myocardial gene expression and stimulation of protein synthesis by putative cardiac growth promoting agents [angiotensin II (AII)/endothelin-1 (E)]. In isolated adult rat ventricular cardiomyocytes, employing northern blotting and hybridization techniques, we observed a significant induction of the transcription factors Egr-1 (Early growth response gene-1) and c-fos by AII and E and an attenuation of this effect by N. AII and E also stimulated total myocardial protein synthesis rates by 108% and 135% respectively; these effects could also be completely inhibited by N. There was a dose-response relationship for the inhibition of the stimulatory effect of E on protein synthesis by N. These data indicate that N could reduce cardiac hypertrophy not depending on any form of haemodynamic overloading. The inhibition of the expression of the oncogenes Egr-1 and c-fos by N may be involved in the attenuation of E- and AII-induced protein synthetic activity in the heart muscle, pointing towards a molecular link between myocardial gene expression and protein synthesis, the latter eventually leading to cardiac hypertrophy.
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