Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Kanda, T. et al.

Myocardial beta-receptor and cardiac angiotensin alterations during the acute and chronic phases of viral myocarditis.

Recovery from viral myocarditis is usually excellent and complete although it occasionally results in sudden death during its acute stage. While neurohormonal mechanisms play an important role in the adaptation to heart diseases, little is known about the alteration of the neurohormonal system in viral myocarditis. Therefore, we examined the myocardial beta-adrenergic receptor and cardiac angiotensin I and II concentrations in a murine model of viral myocarditis induced by an encephalomyocarditis virus. The down-regulation of the beta 1-adrenergic receptor subtype was observed on day 10. The heart weight, heart weight/body weight ratio and myocardial necrosis were significantly increased at this stage. On day 30, the beta 2-adrenergic receptor subtype was up-regulated without up-regulation of the total beta-adrenergic receptor. Both angiotensin I and II concentrations were significantly increased with myocardial hypertrophy in the left ventricle on day 30. The up-regulation of the total beta-adrenergic receptor and beta 2-subtype was observed on day 120, but neither the angiotensin I nor II concentration was increased. Therefore, the up-regulation of the beta 2-adrenergic receptor density and the temporal increase of the angiotensin I and II concentrations in the murine ventricle during viral myocarditis may play an important role in the pathophysiology of post-viral myocarditis.[1]

References

Myocardial beta-receptor and cardiac angiotensin alterations during the acute and chronic phases of viral myocarditis. Kanda, T., Adachi, H., Ohno, T., Suzuki, T., Murata, K. Eur. Heart J. (1994) [Pubmed]

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