title: Effects of physiological or pathological pressure load in vivo on myocardial expression of ET-1 and receptors.
abstract: Endothelin (ET)-1 has potent positive inotropic and chronotropic activity in the heart and induces cardiac hypertrophy. The production of ET-1 in the heart is reported to be increased under some conditions. In normal circulation, the pressure load to the left ventricle (LV) is much greater than that to the right ventricle (RV). In this study, we investigated the gene expression of the myocardial ET-1 system (ET-1, ET(A) receptor, and ET(B) receptor) in the RV and LV of normal rats and also investigated these genes in hypertrophied RV due to pathological pulmonary hypertension (PH). Normal rats showed no differences between the RV and LV in the gene expression of either ET-1, ET(A) receptor, or ET(B) receptor in either the adult stage (11 wk old) or the neonatal stage (1 and 8 days old). On the other hand, the expression of both atrial natriuretic peptide (ANP) mRNA and B-type natriuretic peptide (BNP) mRNA was significantly greater in the LV than in the RV in adult rats. Gene expression of ET-1, ET(A) receptor, and ET(B) receptor in the RV was markedly higher in rats with monocrotaline-induced (pathological) PH than that in control rats. The expression of ANP mRNA and BNP mRNA in the RV was also markedly higher in the rats with PH. In conclusion, the data suggest that gene expression of the ET-1 system in the myocardium is not affected by physiological pressure load in either the adult stage or neonatal stage; however, it is enhanced by pathological pressure overload such as that in PH.
authors.affiliation: Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, Tsukuba, Ibaraki 305-8575, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ueno
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
authors.forename: S
authors.initials: S
authors.lastname: Sakai
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: K
authors.initials: K
authors.lastname: Goto
authors.forename: I
authors.initials: I
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D001794:Blood Pressure / Q000502:physiology*; D018076:DNA, Complementary / Q000378:metabolism; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism*; D016232:Endothelins / Q000235:genetics; D015870:Gene Expression; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D016686:Monocrotaline; D009206:Myocardium / Q000378:metabolism*; D020097:Natriuretic Peptide, Brain; D011498:Protein Precursors / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044022:Receptor, Endothelin A; D044023:Receptor, Endothelin B; D017466:Receptors, Endothelin / Q000235:genetics / Q000378:metabolism*; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
chemical_list: D018076:DNA, Complementary; D019332:Endothelin-1; D016232:Endothelins; D011498:Protein Precursors; D012333:RNA, Messenger; D044022:Receptor, Endothelin A; D044023:Receptor, Endothelin B; D017466:Receptors, Endothelin; D020097:Natriuretic Peptide, Brain; D016686:Monocrotaline; D009320:Atrial Natriuretic Factor