AJP - Endocrinology and Metabolism, Vol 239, Issue 5 372-E378, Copyright © 1980 by American Physiological Society
Polyamine metabolism during cardiac hypertrophy
A. E. Pegg and H. Hibasami
Treatment with thyroxine for 7 days to produce myocardial hypertrophy led
to an increase in the content of putrescine, spermidine, and spermine in
the rat heart. The content of decarboxylated S-adenosylmethionine, the
source of the aminopropyl groups needed for polyamine synthesis, was
increased by the thyroxine treatment as were the activities of ornithine
and S-adenosylmethionine decarboxylases. The enhanced S-adenosylmethionine
decarboxylase activity measured in vitro was due to an increase in the
amount of enzyme protein as measured by immunotitration with a specific
antiserum. In vivo, decarboxylation of S-adenosylmethionine was, therefore,
increased both by the increased amount of enzyme protein and by the
elevated concentration of putrescine (which activates the enzyme) brought
about by the enhanced ornithine carboxylase activity. Spermine synthase did
not change significantly during the treatment and spermidine synthase
increased only slightly. Therefore, the accumulation of polyamines was
mediated predominantly via the increased availability of both putrescine
and decarboxylated S-adenosylmethionine. Administration of
1,3-diamino-2-propanol led to a rapid reduction in the activity of
ornithine decarboxylase in the heart, and continued exposure to this
substance by its inclusion in the drinking water completely prevented the
increase in concentration of putrescine and polyamines in response to
thyroxine. However, cardiac hypertrophy as measured by the increase in
cardiac mass was not prevented by such treatment with 1,3-diaminopropanol,
showing that the increased content of polyamines was not essential for the
hypertrophic response.
