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Increased expression of adrenomedullin 2/intermedin in rat hearts with congestive heart failure
Author(s) -
Hirose Takuo,
Totsune Kazuhito,
Mori Nobuyoshi,
Morimoto Ryo,
Hashimoto Masahiro,
Nakashige Yukiko,
Metoki Hirohito,
Asayama Kei,
Kikuya Masahiro,
Ohkubo Takayoshi,
Hashimoto Junichiro,
Sasano Hironobu,
Kohzuki Masahiro,
Takahashi Kazuhiro,
Imai Yutaka
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.06.020
Subject(s) - adrenomedullin , heart failure , medicine , ventricle , calcitonin , endocrinology , calcitonin gene related peptide , pathophysiology , receptor , cardiology , neuropeptide
Adrenomedullin 2/intermedin (AM2/IMD) is a novel member of the calcitonin/calcitonin gene‐related peptide family. To investigate the pathophysiological role of AM2/IMD in heart failure, we examined the expression of AM2/IMD, adrenomedullin (AM) and receptor complex components (calcitonin receptor‐like receptor, three types of receptor activity‐modifying proteins) by quantitative RT‐PCR and immunohistochemistry in the hearts and kidneys of rats with congestive heart failure (CHF). Significantly increased levels of AM2/IMD mRNAwere found in the atrium, right ventricle, non‐infarcted part of the left ventricle and the infarcted part of the left ventricle of CHF rats, compared with sham operated rats (about 2.8‐fold, 1.7‐fold, 1.7‐fold and 2.5‐fold, respectively). Expression levels of mRNA encoding AM and the receptor complex components were also increased in the hearts of CHF rats. In a separate experiment, AM2/IMD mRNA levels in the heart did not differ between Wistar—Kyoto and spontaneously hypertensive rats. In both sham operated and CHF rats, the myocardium was diffusely immunostained with AM2/IMD. The fibrotic infarcted layer was not immunostained with AM2/IMD but was surrounded by positively immunostained myocardial layers. These findings suggest that the expression of AM2/IMD is enhanced in the failing heart, and AM2/IMD has a certain pathophysiological role in heart failure.