title: Endothelin-converting enzyme and angiotensin-converting enzyme in failing hearts of rats with myocardial infarction.
abstract: We have previously reported that production of endothelin (ET)-1 is markedly increased in failing hearts of rats with chronic heart failure (CHF). It was also reported that the production of angiotensin II (Ang II) is increased in the failing heart. In this study we investigated both converting enzymes of the ET-1 system and the angiotensin system. We used left coronary artery-ligated rats as a model of CHF. The peptide level of ET-1 in the left ventricle (LV) was markedly higher in CHF rats than in control rats. In the LV, expression of preproET-1 mRNA was also markedly higher in CHF rats than in controls. The expression of endothelin-converting enzyme (ECE)-1 mRNA in the rats with CHF was similar to that in controls. Therefore, we believed that the increase in ET-1 production in the failing heart originated from an increase in preproET-1 production rather than increase in ECE. The expression of angiotensin-converting enzyme (ACE) mRNA in failing hearts of CHF rats was significantly higher than that of the sham-operated rats. The expression of angiotensinogen mRNA in failing hearts of these CHF rats was slightly higher than that of the sham-operated rats. This study suggests that there is a difference in the role of peptide synthesis between the ECE system and the ACE system in rats with CHF.
authors.affiliation: Department of Internal Medicine, University of Tsukuba, Ibaraki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
authors.forename: S
authors.initials: S
authors.lastname: Sakai
authors.forename: I
authors.initials: I
authors.lastname: Yamaguchi
authors.forename: K
authors.initials: K
authors.lastname: Goto
authors.forename: Y
authors.initials: Y
authors.lastname: Sugishita
mesh_terms: D000808:Angiotensinogen / Q000096:biosynthesis; D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000096:biosynthesis / Q000378:metabolism*; D019332:Endothelin-1; D000072396:Endothelin-Converting Enzymes; D016232:Endothelins / Q000096:biosynthesis / Q000378:metabolism; D004790:Enzyme Induction / Q000187:drug effects; D006333:Heart Failure / Q000201:enzymology* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D008666:Metalloendopeptidases / Q000096:biosynthesis / Q000378:metabolism*; D009203:Myocardial Infarction / Q000201:enzymology* / Q000503:physiopathology; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D011498:Protein Precursors / Q000096:biosynthesis / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D019332:Endothelin-1; D016232:Endothelins; D011498:Protein Precursors; D012333:RNA, Messenger; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A; D016282:Aspartic Acid Endopeptidases; D008666:Metalloendopeptidases; D000072396:Endothelin-Converting Enzymes