title: The studies of cell damaging and cell growth factors which induce cardiomyopathy.
abstract: We demonstrated that phosphatidylinositide-specific phospholipase C (PLC) activity was greater in cardiomyopathic hamster hearts (BIO 14.6 and BIO 53.58) then in hamster controls (F1b). Inositol trisphosphate (IP3) production was markedly greater in both of the cardiomyopathic hamsters, BIO 14.6 and BIO 53.58. We have also determined the sarcoplasmic reticulum (SR) function of heart. Calcium uptake into SR markedly increased in BIO 14.6. On the other hand, it significantly decreased in BIO 53.58 compared with F1b. It is well known that IP3 stimulates calcium release from SR. In BIO 14.6, calcium release from SR stimulated by IP3 increased, but its effect decreased in BIO 53.58 compared with F1b. These results suggest that PI response may produce high intracellular calcium levels in both BIO 14.6 and BIO 53.58 myocytes. In addition, in the BIO 53.58 hamster the sarcoplasmic reticulum deteriorate in function. It was concluded from these results that a prolonged high intracellular calcium level may lead to the death of BIO 53.58 myocytes. The expression of angiotensinogen mRNA was observed in the hamster heart. There was no differences in its expression level between F1b, BIO 14.6 and BIO 53.58. There was no effect of ages on its expression in these hamster hearts. We have also determined the distribution of angiotensinogen in these hamsters. At 4 weeks of age, the immunohistochemical study revealed that angiotensinogen was widely distributed in subendocardium in these hamsters. There was no difference in its distribution between F1b, BIO 14.6 and BIO 53.58. But at 20 weeks old of age its immunoreactivity decreased in BIO 53.58.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kawaguchi
authors.forename: M
authors.initials: M
authors.lastname: Shoki
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: T
authors.initials: T
authors.lastname: Kudo
authors.forename: H
authors.initials: H
authors.lastname: Sawa
authors.forename: H
authors.initials: H
authors.lastname: Okamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Sakata
authors.forename: H
authors.initials: H
authors.lastname: Yasuda
mesh_terms: D000808:Angiotensinogen / Q000235:genetics / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006224:Cricetinae; D007150:Immunohistochemistry; D008297:Male; D008647:Mesocricetus; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010716:Phosphatidylinositols / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D012084:Renin-Angiotensin System / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D015290:Second Messenger Systems; D010738:Type C Phospholipases / Q000378:metabolism
chemical_list: D010716:Phosphatidylinositols; D012333:RNA, Messenger; D000808:Angiotensinogen; D010738:Type C Phospholipases; D002118:Calcium