Angiotensin II Type 1-Receptor Antagonist Candesartan Cilexitil Prevents Left Ventricular Dysfunction in Myocardial Infarcted Rats.

• Hanatani Akihisa

  First Department of Internal Medicine, Osaka City University Medical School

• Yoshiyama Minoru

  First Department of Internal Medicine, Osaka City University Medical School

• Takeuchi Kazuhide

  First Department of Internal Medicine, Osaka City University Medical School

• Kim Shokei

  Department of Pharmacology, Osaka City University Medical School

• Nakayama Koji

  First Department of Internal Medicine, Osaka City University Medical School

• Omura Takashi

  First Department of Internal Medicine, Osaka City University Medical School

• Iwao Hiroshi

  Department of Pharmacology, Osaka City University Medical School

• Yoshikawa Junichi

  First Department of Internal Medicine, Osaka City University Medical School

書誌事項

タイトル別名

• Angiotensin II Type 1-Receptor Antagoni

抄録

The purpose of this study was to analyze the effect of the angiotensin II type 1-receptor antagonist candesartan cilexitil on left ventricular systolic and diastolic function and mRNA expression of contractile proteins, collagen, and Ca²⁺ handling protein in myocardial-infarcted rats. After myocardial infarction, the animals were randomly assigned to candesartan cilexitil-treated or untreated groups (MI). We performed Doppler-echocardiographic examination and measured the hemodynamics at four and twelve weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. At four weeks in MI, left ventricular end-diastolic dimension increased (Control, 6.2±0.6 mm; MI, 8.7±0.6 mm; P<0.01), fractional shortening decreased (Control, 41±5%; MI, 16±3%; P<0.01) and E wave deceleration rate increased (Control, 14.3±2.0 m/sec²; MI, 23.3±2.3 m/sec²; P<0.01). Candesartan cilexitil significantly prevented these changes. The mRNA expressions of β-myosin heavy chain, α-skeletal actin, atrial natriuretic peptide, and collagens I and III in the non-infarcted left ventricle and right ventricle were increased at four weeks and were significantly suppressed by treatment with candesartan cilexitil. At four weeks, Na⁺-Ca²⁺ exchanger mRNA expression was increased, and candesartan cilexitil suppressed this increase. At twelve weeks, sarcoplasmic reticulum Ca²⁺-ATPase mRNA expression in the infarcted region including the adjacent non-infarcted left ventricle and right ventricle were decreased and candesartan cilexitil restored it to the control level. Candesartan cilexitil prevented the systolic and diastolic dysfunction and abnormal cardiac mRNA expression in myocardial-infarcted rats.

収録刊行物

• Jpn.J.Pharmacol.

  Jpn.J.Pharmacol. 78 (1), 45-54, 1998

  公益社団法人 日本薬理学会

キーワード

• Ventricular remodeling
• Angiotensin II type 1-receptor antagonist
• Echocardiography
• Gene expression
• Diastolic function

詳細情報

• CRID: 1390282679263604992
• NII論文ID: 10008193702
• NII書誌ID: AA00691188
• DOI: 10.1254/jjp.78.45
• COI: 1:CAS:528:DyaK1cXmtlCktbk%3D
• ISSN: 13473506
• ISSN: 00215198
• NDL書誌ID: 4565702
• PubMed: 9804061
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I4565702
• Web Site: https://api.elsevier.com/content/article/PII:S0021519819310674?httpAccept=text/xml
• Web Site: https://api.elsevier.com/content/article/PII:S0021519819310674?httpAccept=text/plain
• Web Site: https://www.jstage.jst.go.jp/article/jjp/78/1/78_1_45/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/1999011048
• 本文言語コード: en
• データソース種別:
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  • NDL
  • Crossref
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  • CiNii Articles
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