Abstract:
:Heart failure (HF) is characterized by abnormalities in beta-adrenergic receptor (betaAR) signaling, including an increase in betaAR kinase 1 (betaARK1) levels and activity. Gene therapy using a peptide inhibitor of betaARK1 (betaARKct) in infarcted rabbit hearts has improved compromised cardiac function. To determine whether betaARK1 inhibition improves survival in a mouse model of HF induced by myocardial infarction (MI), we studied wild-type (WT) and transgenic (TG) mice overexpressing betaARKct following MI. There was no difference in infarct size. Survival of WT mice with MI was 25% at 26 weeks. In contrast, 92% of betaARKct TG mice with MI survived (P = 0.01). betaARKct TG mice with MI at 8 weeks showed significantly higher fractional shortening compared with WT mice with MI (25.1 +/- 2.7% versus 14.2 +/- 1.0%; P < 0.05). Moreover, the biochemical betaAR abnormalities in WT mice with MI were prevented in betaARKct TG mice with MI. In conclusion, betaARK1 inhibition results in a marked increase in survival and improved cardiac function in a mouse model of HF induced by MI.
journal_name
J Cardiovasc Pharmacoljournal_title
Journal of cardiovascular pharmacologyauthors
Suzuki Y,Nakano K,Sugiyama M,Imagawa Jdoi
10.1097/01.fjc.0000134776.70798.44subject
Has Abstractpub_date
2004-09-01 00:00:00pages
329-34issue
3eissn
0160-2446issn
1533-4023pii
00005344-200409000-00009journal_volume
44pub_type
杂志文章abstract::In this report, alterations between the electrical and mechanical responses of isolated neonatal and adult canine ventricular muscle preparations before and after ouabain exposure are described. No significant differences were observed between the two age groups in the concentration-dependent effects of ouabain on inc...
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