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Cardiac natriuretic peptides gene expression and secretion in inflammation.
J Investig Med. 2009 Jan; 57(1):29-32.JI

Abstract

The genetic expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF or ANP) and brain natriuretic peptide (BNP) have been studied mainly in the context of cardiac diseases associated with neuroendocrine and hemodynamic changes arising from cardiac dysfunction such as in chronic congestive heart failure. In this type of pathology, both ANF and BNP plasma levels change in an approximate coordinated fashion so that the use of these hormones as biomarkers of cardiac disease is, in principle, indistinctive. However, we reported that during an acute cardiac allograft rejection episode, BNP plasma levels can significantly increase in the absence of a similar increase in ANF plasma levels. We tested the hypothesis that these changes were related to cytokines and found that some pro-inflammatory cytokines, including TNFalpha and IL-1beta, selectively promote BNP synthesis and secretion in cultures of neonatal rat ventricular cardiocytes. This effect was found related to increased BNP promoter activity and sensitive to p38 mitogen-activated protein kinase inhibition.In order to determine in vivo if the selective up-regulation of BNP would be observed in inflammatory processes other than acute cardiac allograft rejection, we carried out investigation using the experimental autoimmune myocarditis rat model, which histologically resembles human giant cell myocarditis. It was found that this model is also accompanied by a specific increase in BNP-circulating levels although the cytokines involved seem to differ from those characterized earlier through in vitro studies.Recent studies in humans have found that in sepsis, plasma BNP levels increase in the absence of hemodynamic changes.In conclusion, BNP appears to be regulated uniquely in the setting of an inflammatory process. This sets it apart from ANF in terms of potential roles in the pathogenesis of disease and in its use as a biomarker of cardiac disease.

Authors+Show Affiliations

Cardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19158604

Citation

Vesely, David L., and Adolfo J. de Bold. "Cardiac Natriuretic Peptides Gene Expression and Secretion in Inflammation." Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research, vol. 57, no. 1, 2009, pp. 29-32.
Vesely DL, de Bold AJ. Cardiac natriuretic peptides gene expression and secretion in inflammation. J Investig Med. 2009;57(1):29-32.
Vesely, D. L., & de Bold, A. J. (2009). Cardiac natriuretic peptides gene expression and secretion in inflammation. Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research, 57(1), 29-32. https://doi.org/10.2310/JIM.0b013e3181948b37
Vesely DL, de Bold AJ. Cardiac Natriuretic Peptides Gene Expression and Secretion in Inflammation. J Investig Med. 2009;57(1):29-32. PubMed PMID: 19158604.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardiac natriuretic peptides gene expression and secretion in inflammation. AU - Vesely,David L, AU - de Bold,Adolfo J, PY - 2009/1/23/entrez PY - 2009/1/23/pubmed PY - 2009/4/1/medline SP - 29 EP - 32 JF - Journal of investigative medicine : the official publication of the American Federation for Clinical Research JO - J Investig Med VL - 57 IS - 1 N2 - The genetic expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF or ANP) and brain natriuretic peptide (BNP) have been studied mainly in the context of cardiac diseases associated with neuroendocrine and hemodynamic changes arising from cardiac dysfunction such as in chronic congestive heart failure. In this type of pathology, both ANF and BNP plasma levels change in an approximate coordinated fashion so that the use of these hormones as biomarkers of cardiac disease is, in principle, indistinctive. However, we reported that during an acute cardiac allograft rejection episode, BNP plasma levels can significantly increase in the absence of a similar increase in ANF plasma levels. We tested the hypothesis that these changes were related to cytokines and found that some pro-inflammatory cytokines, including TNFalpha and IL-1beta, selectively promote BNP synthesis and secretion in cultures of neonatal rat ventricular cardiocytes. This effect was found related to increased BNP promoter activity and sensitive to p38 mitogen-activated protein kinase inhibition.In order to determine in vivo if the selective up-regulation of BNP would be observed in inflammatory processes other than acute cardiac allograft rejection, we carried out investigation using the experimental autoimmune myocarditis rat model, which histologically resembles human giant cell myocarditis. It was found that this model is also accompanied by a specific increase in BNP-circulating levels although the cytokines involved seem to differ from those characterized earlier through in vitro studies.Recent studies in humans have found that in sepsis, plasma BNP levels increase in the absence of hemodynamic changes.In conclusion, BNP appears to be regulated uniquely in the setting of an inflammatory process. This sets it apart from ANF in terms of potential roles in the pathogenesis of disease and in its use as a biomarker of cardiac disease. SN - 1081-5589 UR - https://www.unboundmedicine.com/medline/citation/19158604/Cardiac_natriuretic_peptides_gene_expression_and_secretion_in_inflammation_ L2 - https://jim.bmj.com/lookup/pmidlookup?view=long&pmid=19158604 DB - PRIME DP - Unbound Medicine ER -