Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat

Abstract

Pressure overload, such as hypertension, to the heart causes pathological cardiac hypertrophy, whereas chronic exercise causes physiological cardiac hypertrophy, which is defined as athletic heart. There are differences in cardiac properties between these two types of hypertrophy. We investigated whether mRNA expression of various cardiovascular regulating factors differs in rat hearts that are physiologically and pathologically hypertrophied, because we hypothesized that these two types of cardiac hypertrophy induce different molecular phenotypes. We used the spontaneously hypertensive rat (SHR group; 19 wk old) as a model of pathological hypertrophy and swim-trained rats (trained group; 19 wk old, swim training for 15 wk) as a model of physiological hypertrophy. We also used sedentary Wistar-Kyoto rats as the control group (19 wk old). Left ventricular mass index for body weight was significantly higher in SHR and trained groups than in the control group. Expression of brain natriuretic peptide, angiotensin-converting enzyme, and endothelin-1 mRNA in the heart was significantly higher in the SHR group than in control and trained groups. Expression of adrenomedullin mRNA in the heart was significantly lower in the trained group than in control and SHR groups. Expression of beta(1)-adrenergic receptor mRNA in the heart was significantly higher in SHR and trained groups than in the control group. Expression of beta(1)-adrenergic receptor kinase mRNA, which inhibits beta(1)-adrenergic receptor activity, in the heart was markedly higher in the SHR group than in control and trained groups. We demonstrated for the first time that the manner of mRNA expression of various cardiovascular regulating factors in the heart differs between physiological and pathological cardiac hypertrophy.

The Insulin-like Growth Factor 1 Receptor Induces Physiological Heart Growth via the Phosphoinositide 3-Kinase(p110α) Pathway

“…pressure or volume overload) or physiological stimuli (e.g. developmental growth, exercise training) (21,(41)(42)(43). Physiological hypertrophy is characterized by a normal organization of cardiac structure, and normal or enhanced cardiac function, whereas pathological hypertrophy is associated with an altered pattern of cardiac gene expression, fibrosis, cardiac dysfunc- tion, and increased morbidity and mortality (44 -47).…”

E2F-1 Regulates the Expression of a Subset of Target Genes during Skeletal Myoblast Hypertrophy

“…The hypertrophic response is initiated by a range of stimuli such as growth factors, hormones, cytokines, vasoactive peptides, and catecholamines (53)(54)(55)(56)(57)(58), and while the intracellular pathways that are activated may distinguish pathologic from physiologic cell growth (59,60) it is likely that these pathways converge on common events affecting cell growth, architecture, and metabolic requirements. We previously demonstrated that several hypertrophic stimuli, including AngII, isoproterenol, prostaglandin F 2␣ , insulin-like growth factor-1, and 1,25-dihydroxyvitamin D 3 , are capable of inducing cell growth without division in C2C12 myoblasts and that all of these result in Rb phosphorylation specifically at serine 780 (10).…”

Cardiac hypertrophy and IGF-1 response to testosterone propionate treatment in trained male rats

“…However, in the experiment in which the age of the animals did not differ we suggested that cardiac hypertrophy can be more accurately quantified by relating HW to BW [3,40,41].…”