Relation between contractile function and regulatory cardiac proteins in hypertrophied hearts. Stein, Birgitt, Sabine Bartel, Uwe Kirchhefer, Sabine Kokott, Ernst -Georg Krause, Joachim Neumann, Wilhelm Schmitz, Hasso Scholz. Abteilung Allgemeine Pharmakologie, Universit[umlaut]ats -Krankenhaus Eppendorf, Martinistra[beta]e 52, 20246 Hamburg, *Max -Delbr[umlaut]uck-Centrum f[umlaut]ur Molekulare Medizin, Robert -R[diaeresis]ossle-Stra[beta]e 10, 13122 Berlin, _Institut f[umlaut]ur Pharmakologie und Toxikologie, Universit[umlaut]at M[umlaut]unster, Domagkstra[beta]e 12, 48149 M[umlaut]unster, FRG
APStracts 2:0540H, 1995.
The aim of the study was to examine the mechanism(s) underlying the reduced isoproterenol-induced positive inotropic and lusitropic effects in hypertrophied hearts. Chronic [beta]-adrenergic stimulation (2.4 mg isoproterenol/kg d; 4 days) induced cardiac hypertrophy by 33+/-2% in rats. Parallel a down-regulation of phospholamban (PLB) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2) protein expression by 49% and 40%, respectively, was observed, whereas troponin I (TNI) and C-protein remained unchanged. In papillary muscles from chronic [beta]-adrenergic stimulated rats the isoproterenol-induced positive inotropic and lusitropic effects as well as cAMP accumulation were attenuated compared to control animals. Acute exposure to isoproterenol induced a phosphate incorporation into PLB, TNI and C-protein of 48+/-4.6, 55+/-5.0 and 27+/-4.9 pmol P/mg homogenate protein, respectively, in control animals. In the hypertrophied hearts only phosphate incorporation into PLB was reduced by 76%, whereas phosphate incorporation into TNI or C-protein remained unchanged. In conclusion, chronic [beta] -adrenergic stimulation reduced the isoproterenol stimulated positive inotropic and lusitropic effects in papillary muscles which were accompanied by i) a diminished cAMP formation ii) an attenuation of cAMP-mediated PLB phosphorylation and iii) a down-regulation of PLB and SERCA2 protein.

Received 13 March 1995; accepted in final form 20 November 1995.
APS Manuscript Number H235-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95