(Hypertension. 2000;36:42.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Increase in Gi
Protein Accompanies Progression of Post-Infarction Remodeling in Hypertensive Cardiomyopathy
From Klinik III (I.K., O.Z., B.C., M.B.) and Klinik II (F.J.) für Innere Medizin, Universität zu Köln, Germany; and Cardiovascular Research, Hoechst Marion Roussel (G.I., W.L.), Frankfurt am Main, Germany.
Correspondence to Prof Dr Michael Böhm, Klinik III für Innere Medizin Universität zu Köln, Joseph-Stelzmann-Str 9, 50924 Köln, Germany. E-mail michael.boehm{at}medizin.uni-koeln.de
Abstract—Hypertensive cardiac
hypertrophy and myocardial infarction (MI) are clinically
relevant risk factors for heart failure. There is no specific
information addressing signaling alterations in the sequence of
hypertrophy and post-MI remodeling. To investigate
alterations in ß-adrenergic receptor G-protein signaling in
ventricular remodeling with pre-existing
hypertrophy, MI was induced by coronary artery
ligation in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats
(SHR). Ten weeks after the induction of MI, the progression of left
ventricular dysfunction and increases in plasma atrial
natriuretic peptide (ANP) and cardiac ANP mRNA were more
pronounced in SHR than WKY. In addition, the impaired contractile
response to ß-adrenergic stimulation was observed in the noninfarcted
papillary muscle isolated from SHR. Immunochemical Gs
protein and ß-adrenoceptor density were not significantly altered by
MI in both strains. However, immunochemical Gi was
increased (1.5-fold) in the noninfarcted left ventricle of the SHR in
which infarction had been induced when compared with that in SHR that
underwent sham operation. This increase was observed especially in rats
with a high plasma ANP level. Furthermore, there was a positive
correlation between Gi and the extent of post-MI
remodeling in WKY. A similar correlation between Gi and
the extent of hypertensive hypertrophy was observed in SHR.
In conclusion, the vulnerability of hypertrophied hearts to
ischemic damage is greater than that of normotensive hearts. An
increase in Gi could be one mechanism involved in the
transition from cardiac hypertrophy to cardiac failure when
chronic pressure overload and loss of contractile mass from
ischemic heart disease coexist.
Key Words: myocardial infarction • cardiomegaly • ventricular remodeling • G proteins • atrial natriuretic factor
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