Format

Send to

Choose Destination
J Cardiovasc Pharmacol. 2010 Jul;56(1):45-52. doi: 10.1097/FJC.0b013e3181ddc785.

Effect of intermedin1-53 on angiotensin II-induced hypertrophy in neonatal rat ventricular myocytes.

Author information

1
Institute of Brain Science, Shanxi Datong University School of Medical Science, Datong, Shanxi, PR China.

Abstract

OBJECTIVES:

Intermedin (IMD) is coexpressed in the heart with its receptor, which suggests that it may have localized actions as a modulator of cardiac function. The present study was designed to observe the interaction between IMD and cardiac hypertrophy and the possible mechanism involved in the antihypertrophic effects of IMD1-53 in cultured neonatal ventricular myocytes.

METHODS:

Myocyte hypertrophy was induced by treating the cells with angiotensin II, and the hypertrophic response was characterized by a significant increase in cell surface area, protein synthesis, and BNP mRNA expression.

RESULTS:

Our results showed that angiotensin II led to an obvious decrease in the production, secretion, and mRNA expression of IMD and increase receptor activity modifying proteins 1, 3 mRNA expression. Moreover, IMD1-53 inhibited the angiotensin II-induced hypertrophic response and the effects of IMD1-53 were similar to those of equivalent-dose adrenomedullin and could been blocked by H89. Otherwise, in our study, IMD1-53 resulted in dose-dependent increases of cAMP production in cardiomyocytes.

CONCLUSIONS:

Thus, IMD and its receptor system are involved in cardiac hypertrophy, and like adrenomedullin, IMD1-53 exerts an antihypertrophic effect on neonatal cardiomyocytes and the effect can be mediated by the cAMP/PKA pathway.

PMID:
20351561
DOI:
10.1097/FJC.0b013e3181ddc785
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center