Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction

Norio Hama, Hiroshi Itoh, Gotaro Shirakami, Osamu Nakagawa, Shin Ichi Suga, Yoshihiro Ogawa, Izuru Masuda, Kuniaki Nakanishi, Takaaki Yoshimasa, Yukiya Hashimoto, Masayuki Yamaguchi, Ryouhei Hori, Hirofumi Yasue, Kazuwa Nakao

Research output: Contribution to journalArticle

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Abstract

Background: We have demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone predominantly synthesized in and secreted from the ventricle. We have also reported that, compared with atrial natriuretic peptide (ANP), the plasma concentration of BNP is increased to a greater degree in patients with congestive heart failure and more rapidly in patients with acute myocardial infarction (AMI). Methods and Results: To investigate ventricular gent expression of BNP in AMI, we analyzed plasma and ventricular BNP concentrations along with ventricular BNP mRNA in rats with AMI produced by coronary artery ligation. The BNP concentration in the left ventricle increased about 2-fold as early as 12 hours postinfarction and 5-fold 1 day postinfarction compared with sham-operated rats, whereas left ventricular ANP concentration remained unchanged within 1 day. The tissue concentration of BNP increased in the noninfarcted region as well as in the infarcted region. The surviving myocytes in and around the necrotic tissues in the infarcted region were intensely stained with the anti-BNP antiserum, indicating augmented production in the remaining myocytes in the infarcts. The BNP concentration in the right ventricle also increased about 10-fold 12 hours postinfarction, whereas the ANP concentration remained unchanged within 12 hours. Northern blot analysis revealed that BNP mRNA expression was augmented 3-fold in the left ventricle as early as 4 hours postinfarction. In contrast, ANP mRNA expression was unchanged. Reflecting the rapid induction of ventricular BNP production, the plasma BNP concentration rose to about 100 pg/mL 12 hours postinfarction (sham-operated rats, <70 pg/mL). Conclusions: These results demonstrate the rapid induction of ventricular BNP gene expression in rats with AMI compared with ANP and suggest that BNP gene expression in the ventricle is regulated distinctively from ANP gene expression against acute ventricular overload. They also suggest that the BNP gene can be one of the acutely responsive cardiac genes for the ventricular overload and suggest a possible pathophysiological role of BNP distinct from ANP in AMI.

Original languageEnglish
Pages (from-to)1558-1564
Number of pages7
JournalCirculation
Volume92
Issue number6
DOIs
Publication statusPublished - Sep 15 1995
Externally publishedYes

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Brain Natriuretic Peptide
Myocardial Infarction
Gene Expression
Atrial Natriuretic Factor
Heart Ventricles
Muscle Cells
Messenger RNA
Northern Blotting
Genes

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction. / Hama, Norio; Itoh, Hiroshi; Shirakami, Gotaro; Nakagawa, Osamu; Suga, Shin Ichi; Ogawa, Yoshihiro; Masuda, Izuru; Nakanishi, Kuniaki; Yoshimasa, Takaaki; Hashimoto, Yukiya; Yamaguchi, Masayuki; Hori, Ryouhei; Yasue, Hirofumi; Nakao, Kazuwa.

In: Circulation, Vol. 92, No. 6, 15.09.1995, p. 1558-1564.

Research output: Contribution to journalArticle

Hama, N, Itoh, H, Shirakami, G, Nakagawa, O, Suga, SI, Ogawa, Y, Masuda, I, Nakanishi, K, Yoshimasa, T, Hashimoto, Y, Yamaguchi, M, Hori, R, Yasue, H & Nakao, K 1995, 'Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction', Circulation, vol. 92, no. 6, pp. 1558-1564. https://doi.org/10.1161/01.CIR.92.6.1558
Hama, Norio ; Itoh, Hiroshi ; Shirakami, Gotaro ; Nakagawa, Osamu ; Suga, Shin Ichi ; Ogawa, Yoshihiro ; Masuda, Izuru ; Nakanishi, Kuniaki ; Yoshimasa, Takaaki ; Hashimoto, Yukiya ; Yamaguchi, Masayuki ; Hori, Ryouhei ; Yasue, Hirofumi ; Nakao, Kazuwa. / Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction. In: Circulation. 1995 ; Vol. 92, No. 6. pp. 1558-1564.
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abstract = "Background: We have demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone predominantly synthesized in and secreted from the ventricle. We have also reported that, compared with atrial natriuretic peptide (ANP), the plasma concentration of BNP is increased to a greater degree in patients with congestive heart failure and more rapidly in patients with acute myocardial infarction (AMI). Methods and Results: To investigate ventricular gent expression of BNP in AMI, we analyzed plasma and ventricular BNP concentrations along with ventricular BNP mRNA in rats with AMI produced by coronary artery ligation. The BNP concentration in the left ventricle increased about 2-fold as early as 12 hours postinfarction and 5-fold 1 day postinfarction compared with sham-operated rats, whereas left ventricular ANP concentration remained unchanged within 1 day. The tissue concentration of BNP increased in the noninfarcted region as well as in the infarcted region. The surviving myocytes in and around the necrotic tissues in the infarcted region were intensely stained with the anti-BNP antiserum, indicating augmented production in the remaining myocytes in the infarcts. The BNP concentration in the right ventricle also increased about 10-fold 12 hours postinfarction, whereas the ANP concentration remained unchanged within 12 hours. Northern blot analysis revealed that BNP mRNA expression was augmented 3-fold in the left ventricle as early as 4 hours postinfarction. In contrast, ANP mRNA expression was unchanged. Reflecting the rapid induction of ventricular BNP production, the plasma BNP concentration rose to about 100 pg/mL 12 hours postinfarction (sham-operated rats, <70 pg/mL). Conclusions: These results demonstrate the rapid induction of ventricular BNP gene expression in rats with AMI compared with ANP and suggest that BNP gene expression in the ventricle is regulated distinctively from ANP gene expression against acute ventricular overload. They also suggest that the BNP gene can be one of the acutely responsive cardiac genes for the ventricular overload and suggest a possible pathophysiological role of BNP distinct from ANP in AMI.",
author = "Norio Hama and Hiroshi Itoh and Gotaro Shirakami and Osamu Nakagawa and Suga, {Shin Ichi} and Yoshihiro Ogawa and Izuru Masuda and Kuniaki Nakanishi and Takaaki Yoshimasa and Yukiya Hashimoto and Masayuki Yamaguchi and Ryouhei Hori and Hirofumi Yasue and Kazuwa Nakao",
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T1 - Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction

AU - Hama, Norio

AU - Itoh, Hiroshi

AU - Shirakami, Gotaro

AU - Nakagawa, Osamu

AU - Suga, Shin Ichi

AU - Ogawa, Yoshihiro

AU - Masuda, Izuru

AU - Nakanishi, Kuniaki

AU - Yoshimasa, Takaaki

AU - Hashimoto, Yukiya

AU - Yamaguchi, Masayuki

AU - Hori, Ryouhei

AU - Yasue, Hirofumi

AU - Nakao, Kazuwa

PY - 1995/9/15

Y1 - 1995/9/15

N2 - Background: We have demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone predominantly synthesized in and secreted from the ventricle. We have also reported that, compared with atrial natriuretic peptide (ANP), the plasma concentration of BNP is increased to a greater degree in patients with congestive heart failure and more rapidly in patients with acute myocardial infarction (AMI). Methods and Results: To investigate ventricular gent expression of BNP in AMI, we analyzed plasma and ventricular BNP concentrations along with ventricular BNP mRNA in rats with AMI produced by coronary artery ligation. The BNP concentration in the left ventricle increased about 2-fold as early as 12 hours postinfarction and 5-fold 1 day postinfarction compared with sham-operated rats, whereas left ventricular ANP concentration remained unchanged within 1 day. The tissue concentration of BNP increased in the noninfarcted region as well as in the infarcted region. The surviving myocytes in and around the necrotic tissues in the infarcted region were intensely stained with the anti-BNP antiserum, indicating augmented production in the remaining myocytes in the infarcts. The BNP concentration in the right ventricle also increased about 10-fold 12 hours postinfarction, whereas the ANP concentration remained unchanged within 12 hours. Northern blot analysis revealed that BNP mRNA expression was augmented 3-fold in the left ventricle as early as 4 hours postinfarction. In contrast, ANP mRNA expression was unchanged. Reflecting the rapid induction of ventricular BNP production, the plasma BNP concentration rose to about 100 pg/mL 12 hours postinfarction (sham-operated rats, <70 pg/mL). Conclusions: These results demonstrate the rapid induction of ventricular BNP gene expression in rats with AMI compared with ANP and suggest that BNP gene expression in the ventricle is regulated distinctively from ANP gene expression against acute ventricular overload. They also suggest that the BNP gene can be one of the acutely responsive cardiac genes for the ventricular overload and suggest a possible pathophysiological role of BNP distinct from ANP in AMI.

AB - Background: We have demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone predominantly synthesized in and secreted from the ventricle. We have also reported that, compared with atrial natriuretic peptide (ANP), the plasma concentration of BNP is increased to a greater degree in patients with congestive heart failure and more rapidly in patients with acute myocardial infarction (AMI). Methods and Results: To investigate ventricular gent expression of BNP in AMI, we analyzed plasma and ventricular BNP concentrations along with ventricular BNP mRNA in rats with AMI produced by coronary artery ligation. The BNP concentration in the left ventricle increased about 2-fold as early as 12 hours postinfarction and 5-fold 1 day postinfarction compared with sham-operated rats, whereas left ventricular ANP concentration remained unchanged within 1 day. The tissue concentration of BNP increased in the noninfarcted region as well as in the infarcted region. The surviving myocytes in and around the necrotic tissues in the infarcted region were intensely stained with the anti-BNP antiserum, indicating augmented production in the remaining myocytes in the infarcts. The BNP concentration in the right ventricle also increased about 10-fold 12 hours postinfarction, whereas the ANP concentration remained unchanged within 12 hours. Northern blot analysis revealed that BNP mRNA expression was augmented 3-fold in the left ventricle as early as 4 hours postinfarction. In contrast, ANP mRNA expression was unchanged. Reflecting the rapid induction of ventricular BNP production, the plasma BNP concentration rose to about 100 pg/mL 12 hours postinfarction (sham-operated rats, <70 pg/mL). Conclusions: These results demonstrate the rapid induction of ventricular BNP gene expression in rats with AMI compared with ANP and suggest that BNP gene expression in the ventricle is regulated distinctively from ANP gene expression against acute ventricular overload. They also suggest that the BNP gene can be one of the acutely responsive cardiac genes for the ventricular overload and suggest a possible pathophysiological role of BNP distinct from ANP in AMI.

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