title: 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.
authors.affiliation: Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-0006, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Iemitsu
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
authors.forename: S
authors.initials: S
authors.lastname: Maeda
authors.forename: S
authors.initials: S
authors.lastname: Sakai
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: N
authors.initials: N
authors.lastname: Fujii
authors.forename: H
authors.initials: H
authors.lastname: Miyazaki
authors.forename: M
authors.initials: M
authors.lastname: Matsuda
authors.forename: I
authors.initials: I
authors.lastname: Yamaguchi
mesh_terms: D000199:Actins / Q000235:genetics; D053607:Adrenomedullin; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight; D006332:Cardiomegaly / Q000235:genetics* / Q000473:pathology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D020097:Natriuretic Peptide, Brain / Q000235:genetics*; D010455:Peptides / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D043585:Receptor, Muscarinic M2; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics*; D011976:Receptors, Muscarinic / Q000235:genetics*; D012016:Reference Values; D013550:Swimming; D014158:Transcription, Genetic
chemical_list: D000199:Actins; D010455:Peptides; D043585:Receptor, Muscarinic M2; D018342:Receptors, Adrenergic, beta-1; D011976:Receptors, Muscarinic; D020097:Natriuretic Peptide, Brain; D053607:Adrenomedullin; D007703:Peptidyl-Dipeptidase A