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Gene Review

Nppb  -  natriuretic peptide B

Rattus norvegicus

Synonyms: BNP, Bnf, Gamma-brain natriuretic peptide, Iso-ANP, Natriuretic peptides B
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Disease relevance of Nppb


High impact information on Nppb

  • Application of mechanical strain to neonatal rat ventricular myocytes in culture evokes changes in gene expression reminiscent of those that occur with hypertrophy in vivo, such as stimulation of brain natriuretic peptide (BNP) gene expression [6].
  • This activation may play an important role in signaling the increased BNP gene expression that accompanies hemodynamic overload and cardiac hypertrophy in vivo [6].
  • Both atrial and brain natriuretic peptides (ANP, BNP), which activate particulate guanylate cyclase, inhibited ppET-1 mRNA expression and [3H]thymidine incorporation stimulated by ANG II and ET-1 [7].
  • During cardiocyte hypertrophy evoked by endothelin-1, Phenylephrine, or PMA, the steady state level of BNP mRNA increased as rapidly as the "immediate-early" induction of the c-fos gene expression, and reached a maximal level within 1 h [8].
  • In hamsters, BNP and ANP occur mainly in the ventricle and the atrium, respectively [9].

Chemical compound and disease context of Nppb


Biological context of Nppb


Anatomical context of Nppb

  • In this study, reporter constructs transfected into neonatal rat ventricular myocytes showed that in the context of 2.5 kilobase pairs of native BNP 5'-flanking sequences, a 2-base pair mutation in a promoter-proximal M-CAT site (CATTCT) disrupted basal and PE-inducible transcription by more than 98% [16].
  • Thus BNP, which increases cyclic GMP independently of NO, is an important approach to prevent growth in the diabetic myocardium, where endothelium-dependent mechanisms are compromised [17].
  • To study the molecular mechanisms for load-induced activation of BNP gene expression, increased wall stress was imposed on isolated isovolumetrically beating adult rat hearts by distension of a fluid filled balloon within the left ventricle [18].
  • Progressive cardiac hypertrophy was accompanied by increased ANP mRNA prevalence throughout the heart and increased BNP mRNA in the left atrium [3].
  • METHODS AND RESULTS: To investigate ventricular gene 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 [4].

Associations of Nppb with chemical compounds

  • Although inducible elements in the ANP gene have been identified, responsible elements in the BNP gene are unknown [16].
  • However, the blunting of hypertrophic markers and accompanying increases in cyclic GMP stimulated by BNP were preserved in diabetes [17].
  • Isolated M-CAT elements conferred PE, protein kinase C, and Ras inducibility to a minimal BNP promoter, however, they did not confer Raf-1 inducibility [16].
  • LPS-mediated BNP expression was completely inhibited by the pretreatment of SB203580, a specific inhibitor for p38 MAPK as well as by genistein, a broad range tyrosine kinase inhibitor [15].
  • The MLR-induced increases in BNP secretion were completely abolished by SB203580 pre-treatment [19].

Regulatory relationships of Nppb

  • The mixed endothelin-1 ET(A)/ET(B) receptor antagonist bosentan but not the angiotensin II type 1 receptor antagonist losartan completely inhibited the pressure overload-induced increase in left ventricular BNP GATA4 binding activity [20].

Other interactions of Nppb

  • Cotransfection of the expression vectors for constitutive active forms of Rac1, MKK3 and p38 MAPK significantly increased BNP promoter activity [15].
  • There was no correlation between the Nppa or Nppb genes or other markers in this region and either heart weight or left ventricular weight in F2 rats [1].
  • Several of the genes upregulated in the hypertrophied heart, including B-type natriuretic peptide (BNP) gene, are controlled by the cardiac-restricted zinc finger transcription factor GATA4 [20].
  • ANF, BNP, as well as alpha- and beta-myosin heavy chain (MHC) mRNA were estimated by Northern blot analysis [21].
  • Pressure overload within 15 to 60 minutes produced an increase in left ventricular BNP GATA4 but not GATA5 and GATA6 binding activity, and at 30 minutes a 2.2-fold increase (P:<0.001) in GATA4 binding was noted [20].

Analytical, diagnostic and therapeutic context of Nppb

  • Northern blot analysis showed that LPS induces the expression of the BNP gene [15].
  • This study tested pro-inflammatory cytokines or conditioned medium (CM) derived from mixed- lymphocyte reaction (MLR) cultures in their ability to modulate ANF or BNP mRNA expression, secretion, as well as BNP promoter activity in cultured neonatal rat cardiocytes [19].
  • An increase in circulating brain natriuretic peptide (BNP) but not atrial natriuretic factor (ANF) is observed coincident with cardiac allograft rejection that is reversed upon treatment with anti-lymphocyte therapy suggesting that pro-inflammatory cytokines may uniquely modulate BNP gene expression and secretion [19].
  • By using a radioimmunoassay (RIA) system newly established for rat BNP, a high concentration of ir-BNP was found to exist in rat cardiac atrium [22].
  • Two ir-BNPs of different molecular weights (11K and 5K) were isolated from rat cardiac atria by anti-rat BNP IgG immunoaffinity chromatography and reverse phase high performance liquid chromatography (HPLC) [22].


  1. Cosegregation analysis of natriuretic peptide genes and blood pressure in the spontaneously hypertensive rat. Ye, P., West, M.J. Clin. Exp. Pharmacol. Physiol. (2003) [Pubmed]
  2. Triiodothyronine increases brain natriuretic peptide (BNP) gene transcription and amplifies endothelin-dependent BNP gene transcription and hypertrophy in neonatal rat ventricular myocytes. Liang, F., Webb, P., Marimuthu, A., Zhang, S., Gardner, D.G. J. Biol. Chem. (2003) [Pubmed]
  3. Differential regulation of natriuretic peptide receptor messenger RNAs during the development of cardiac hypertrophy in the rat. Brown, L.A., Nunez, D.J., Wilkins, M.R. J. Clin. Invest. (1993) [Pubmed]
  4. Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction. Hama, N., Itoh, H., Shirakami, G., Nakagawa, O., Suga, S., Ogawa, Y., Masuda, I., Nakanishi, K., Yoshimasa, T., Hashimoto, Y. Circulation (1995) [Pubmed]
  5. Overexpression of brain natriuretic peptide in mice ameliorates immune-mediated renal injury. Suganami, T., Mukoyama, M., Sugawara, A., Mori, K., Nagae, T., Kasahara, M., Yahata, K., Makino, H., Fujinaga, Y., Ogawa, Y., Tanaka, I., Nakao, K. J. Am. Soc. Nephrol. (2001) [Pubmed]
  6. Mechanical strain activates BNP gene transcription through a p38/NF-kappaB-dependent mechanism. Liang, F., Gardner, D.G. J. Clin. Invest. (1999) [Pubmed]
  7. Natriuretic peptides inhibit angiotensin II-induced proliferation of rat cardiac fibroblasts by blocking endothelin-1 gene expression. Fujisaki, H., Ito, H., Hirata, Y., Tanaka, M., Hata, M., Lin, M., Adachi, S., Akimoto, H., Marumo, F., Hiroe, M. J. Clin. Invest. (1995) [Pubmed]
  8. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload. Nakagawa, O., Ogawa, Y., Itoh, H., Suga, S., Komatsu, Y., Kishimoto, I., Nishino, K., Yoshimasa, T., Nakao, K. J. Clin. Invest. (1995) [Pubmed]
  9. Molecular cloning of hamster brain and atrial natriuretic peptide cDNAs. Cardiomyopathic hamsters are useful models for brain and atrial natriuretic peptides. Tamura, N., Ogawa, Y., Itoh, H., Arai, H., Suga, S., Nakagawa, O., Komatsu, Y., Kishimoto, I., Takaya, K., Yoshimasa, T. J. Clin. Invest. (1994) [Pubmed]
  10. Epigallocathechin-3 gallate inhibits cardiac hypertrophy through blocking reactive oxidative species-dependent and -independent signal pathways. Li, H.L., Huang, Y., Zhang, C.N., Liu, G., Wei, Y.S., Wang, A.B., Liu, Y.Q., Hui, R.T., Wei, C., Williams, G.M., Liu, D.P., Liang, C.C. Free Radic. Biol. Med. (2006) [Pubmed]
  11. Posttranscriptional control of BNP gene expression in angiotensin II-induced hypertension. Suo, M., Hautala, N., Földes, G., Szokodi, I., Tóth, M., Leskinen, H., Uusimaa, P., Vuolteenaho, O., Nemer, M., Ruskoaho, H. Hypertension (2002) [Pubmed]
  12. Evidence for load-dependent and load-independent determinants of cardiac natriuretic peptide production. Ogawa, T., Linz, W., Stevenson, M., Bruneau, B.G., Kuroski de Bold, M.L., Chen, J.H., Eid, H., Schölkens, B.A., de Bold, A.J. Circulation (1996) [Pubmed]
  13. Accelerated secretion of brain natriuretic peptide from the hypertrophied ventricles in experimental malignant hypertension. Kohno, M., Horio, T., Yoshiyama, M., Takeda, T. Hypertension (1992) [Pubmed]
  14. Regulation of rat brain natriuretic peptide transcription. A potential role for GATA-related transcription factors in myocardial cell gene expression. Thuerauf, D.J., Hanford, D.S., Glembotski, C.C. J. Biol. Chem. (1994) [Pubmed]
  15. Transcriptional activation of the BNP gene by lipopolysaccharide is mediated through GATA elements in neonatal rat cardiac myocytes. Tomaru Ki, K., Arai, M., Yokoyama, T., Aihara, Y., Sekiguchi Ki, K., Tanaka, T., Nagai, R., Kurabayashi, M. J. Mol. Cell. Cardiol. (2002) [Pubmed]
  16. Differential effects of protein kinase C, Ras, and Raf-1 kinase on the induction of the cardiac B-type natriuretic peptide gene through a critical promoter-proximal M-CAT element. Thuerauf, D.J., Glembotski, C.C. J. Biol. Chem. (1997) [Pubmed]
  17. B-type natriuretic peptide prevents acute hypertrophic responses in the diabetic rat heart: importance of cyclic GMP. Rosenkranz, A.C., Hood, S.G., Woods, R.L., Dusting, G.J., Ritchie, R.H. Diabetes (2003) [Pubmed]
  18. Posttranscriptional activation of BNP gene expression in response to increased left ventricular wall stress: role of calcineurin and PKC. Tenhunen, O., Szokodi, I., Ruskoaho, H. Regul. Pept. (2005) [Pubmed]
  19. Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by pro-inflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase. Ma, K.K., Ogawa, T., de Bold, A.J. J. Mol. Cell. Cardiol. (2004) [Pubmed]
  20. Pressure overload increases GATA4 binding activity via endothelin-1. Hautala, N., Tokola, H., Luodonpää, M., Puhakka, J., Romppanen, H., Vuolteenaho, O., Ruskoaho, H. Circulation (2001) [Pubmed]
  21. Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development. Kuroski de Bold, M.L. Am. J. Hypertens. (1998) [Pubmed]
  22. Isolation and identification of rat brain natriuretic peptides in cardiac atrium. Aburaya, M., Hino, J., Minamino, N., Kangawa, K., Matsuo, H. Biochem. Biophys. Res. Commun. (1989) [Pubmed]
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