Hypertension, Vol 20, 103-112, Copyright © 1992 by American Heart Association
M Bohm, P Gierschik, A Knorr, K Larisch, K Weismann and E Erdmann
The present study investigated whether reduced adenylate cyclase activity
and an increase in inhibitory guanine nucleotide binding proteins (Gi
alpha), which have been observed in the failing human heart, already occur
in myocardial hypertrophy before the stage of heart failure. In membranes
of hypertrophic hearts from rats with different forms of experimentally
induced hypertension without heart failure (one-kidney, one clip rats,
deoxycorticosterone-treated rats, and rats with reduced renal mass), basal
as well as isoprenaline-, 5'- guanylylimidodiphosphate-, and
forskolin-stimulated adenylate cyclase activity was reduced. The activity
of the catalyst was depressed in deoxycorticosterone but unchanged in
one-kidney, one clip and reduced renal mass compared with controls. The
number of beta-adrenergic receptors was similar in all groups.
Radioimmunological quantification of Gi alpha proteins revealed an increase
by 73% in one-kidney, one clip, 67% in reduced renal mass, but only 20% in
deoxycorticosterone compared with sham-operated, age-matched control rats.
The increase of Gi alpha was accompanied by smaller changes of pertussis
toxin-induced [32P]ADP-ribosylation of a 40-kd membrane protein. It is
concluded that Gi alpha contributes to the reduced adenylate cyclase
activity in cardiac hypertrophy in one-kidney, one clip and reduced renal
mass and to a smaller extent in deoxycorticosterone. It is suggested that
an enhanced expression of Gi alpha could occur not only in severe heart
failure but also in cardiac hypertrophy and could, therefore, contribute to
myocardial depression and progression of disease in heart failure. In
addition, Gi alpha might represent an important regulatory mechanism for
cardiac adenylate cyclase activity and thus, might play an important role
in various cardiac diseases.
ARTICLES
Desensitization of adenylate cyclase and increase of Gi alpha in cardiac hypertrophy due to acquired hypertension
Medizinische Klinik I, Universitat Munchen, Germany.
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