The induction of cardiac hypertrophy by catecholamines can be dissociated from their inotropic effect.
In this study, ornithine decarboxylase, the first and rate-limiting enzyme of the polyamine pathway, was used as a marker of the very early stages of cardiac hypertrophy. Our data show that ornithine decarboxylase is independently regulated by ventricular wall stress and adrenergic receptors, and support the theory that catecholamines have a pressure-independent trophic effect. The infusion of beta 2-adrenergic agonist, terbutaline, at 10(-7) mol/l, did not affect the cardiac performance of isovolumic perfused rat hearts. Despite the lack of functional changes, ornithine decarboxylase activity, as assayed in vitro by 14C-ornithine decarboxylation, was markedly increased in both left and right ventricles. Further investigation showed that ornithine decarboxylase stimulation by catecholamines, unlike ornithine decarboxylase basal activity, was dependent on the extracellular calcium level. Furthermore, passive increases in ventricular wall stress in non-beating hearts also increased left ventricular ornithine decarboxylase activity.
Carlier
P G
PG
Département de Médecine, Université de Liège, Belgium.
Gilles
R J
RJ
Smelten
N S
NS
Yerna
N M
NM
Rorive
G L
GL
D000818:Animals; D006332:Cardiomegaly / Q000201:enzymology / Q000209:etiology*; D006439:Hemodynamics / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects*; D009955:Ornithine Decarboxylase / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D013314:Stress, Mechanical; D013726:Terbutaline / Q000494:pharmacology*
D009955:Ornithine Decarboxylase; D013726:Terbutaline