Circulation, Vol 82, 1249-1265, Copyright © 1990 by American Heart Association
M Bohm, P Gierschik, KH Jakobs, B Pieske, P Schnabel, M Ungerer and E Erdmann
In myocardial membranes from hearts with dilated cardiomyopathy (DCM),
there was a 37% increase of the Gi alpha-protein as measured by 32P-ADP-
ribosylation of a approximately 40 kDa pertussis toxin substrate.
Immunoblotting techniques also showed increased amounts of Gi alpha in DCM.
In hearts with ischemic cardiomyopathy (ICM), Gi alpha was not altered
compared with nonfailing myocardium (NF). Basal and Gpp(NH)p- stimulated
adenylate cyclase activity was reduced in DCM but not in ICM. The number of
beta-adrenoceptors was similarly reduced both in DCM and ICM compared with
NF. Alterations of m-cholinoceptors or A1- adenosine receptors did not
occur. Consistently, "indirect" negative inotropic effects of the
m-cholinoceptor agonist carbachol and the A1- adenosine receptor agonist
R-PIA were not different in ICM, DCM, and nonfailing myocardium. In ICM and
DCM, there was a marked reduction of the positive inotropic responses to
isoprenaline and milrinone. However, there was a further reduction in DCM
compared with ICM. It is concluded that the increase of Gi alpha is
accompanied by a reduction of basal and guanine-nucleotide-stimulated
adenylate cyclase activity. Alterations of m-cholinoceptors and
A1-adenosine receptors do not appear to be involved. The further decrease
of the positive inotropic effects of isoprenaline and milrinone in DCM
provides evidence that the increase of Gi alpha is functionally relevant in
DCM but not ICM and hence might contribute to the reduced effects of
endogenous catecholamines and exogenous cAMP-dependent positive inotropic
agents in the former but not the latter condition.
ARTICLES
Increase of Gi alpha in human hearts with dilated but not ischemic cardiomyopathy
Medizinische Klinik I, Universitat Munchen, FRG.
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