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Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis.
Am J Physiol Heart Circ Physiol. 2008 Jun; 294(6):H2596-603.AJ

Abstract

The cardiac natriuretic peptides atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are discoordinately regulated in myocardial inflammation associated with acute allograft rejection in humans and during in vitro exposure of cardiocyte cultures to some proinflammatory cytokines. We used experimental autoimmune myocarditis (EAM) to determine whether the discoordinate regulation of ANF and BNP was specific to the situations above or was generally associated with other types of myocardial inflammation. The dependency of this process to angiotensin signaling was also determined, given that previous work demonstrated beneficial effects of the angiotensin receptor blocker olmesartan in myocarditis. Histopathological changes, plasma and cardiac ANF, BNP, and selected cytokines gene expression as well as plasma cytokine levels using a cytokine array were determined in EAM, angiotensin receptor blocker-treated, and control rats. It was found that EAM specifically increases BNP but not ANF circulating levels, thus mimicking the findings in acute cardiac allograft rejection and the effect of some proinflammatory cytokines on cardiocyte cultures in vitro. Plasma cytokine array and real-time PCR revealed that lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, and tissue inhibitor of metalloproteinase-1 were increased in plasma and in the myocardium of EAM rats. Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM, thus providing a mechanistic insight into this phenomenon. It is concluded that the inflammatory process contributes specific cytokines, leading to the disregulation of cardiac ANF and BNP production observed during myocardial inflammation, and that this process is angiotensin receptor 1 dependent.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18408131

Citation

Ogawa, Tsuneo, et al. "Angiotensin II Receptor Antagonism Reverts the Selective Cardiac BNP Upregulation and Secretion Observed in Myocarditis." American Journal of Physiology. Heart and Circulatory Physiology, vol. 294, no. 6, 2008, pp. H2596-603.
Ogawa T, Veinot JP, Kuroski de Bold ML, et al. Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis. Am J Physiol Heart Circ Physiol. 2008;294(6):H2596-603.
Ogawa, T., Veinot, J. P., Kuroski de Bold, M. L., Georgalis, T., & de Bold, A. J. (2008). Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis. American Journal of Physiology. Heart and Circulatory Physiology, 294(6), H2596-603. https://doi.org/10.1152/ajpheart.00215.2008
Ogawa T, et al. Angiotensin II Receptor Antagonism Reverts the Selective Cardiac BNP Upregulation and Secretion Observed in Myocarditis. Am J Physiol Heart Circ Physiol. 2008;294(6):H2596-603. PubMed PMID: 18408131.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis. AU - Ogawa,Tsuneo, AU - Veinot,John P, AU - Kuroski de Bold,Mercedes L, AU - Georgalis,Tina, AU - de Bold,Adolfo J, Y1 - 2008/04/11/ PY - 2008/4/15/pubmed PY - 2008/8/16/medline PY - 2008/4/15/entrez SP - H2596 EP - 603 JF - American journal of physiology. Heart and circulatory physiology JO - Am J Physiol Heart Circ Physiol VL - 294 IS - 6 N2 - The cardiac natriuretic peptides atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are discoordinately regulated in myocardial inflammation associated with acute allograft rejection in humans and during in vitro exposure of cardiocyte cultures to some proinflammatory cytokines. We used experimental autoimmune myocarditis (EAM) to determine whether the discoordinate regulation of ANF and BNP was specific to the situations above or was generally associated with other types of myocardial inflammation. The dependency of this process to angiotensin signaling was also determined, given that previous work demonstrated beneficial effects of the angiotensin receptor blocker olmesartan in myocarditis. Histopathological changes, plasma and cardiac ANF, BNP, and selected cytokines gene expression as well as plasma cytokine levels using a cytokine array were determined in EAM, angiotensin receptor blocker-treated, and control rats. It was found that EAM specifically increases BNP but not ANF circulating levels, thus mimicking the findings in acute cardiac allograft rejection and the effect of some proinflammatory cytokines on cardiocyte cultures in vitro. Plasma cytokine array and real-time PCR revealed that lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, and tissue inhibitor of metalloproteinase-1 were increased in plasma and in the myocardium of EAM rats. Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM, thus providing a mechanistic insight into this phenomenon. It is concluded that the inflammatory process contributes specific cytokines, leading to the disregulation of cardiac ANF and BNP production observed during myocardial inflammation, and that this process is angiotensin receptor 1 dependent. SN - 0363-6135 UR - https://www.unboundmedicine.com/medline/citation/18408131/Angiotensin_II_receptor_antagonism_reverts_the_selective_cardiac_BNP_upregulation_and_secretion_observed_in_myocarditis_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.00215.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -