Premium
THE ROLE OF THE OPIOIDERGIC SYSTEM IN A FAMILIAL MODEL OF DILATED CARDIOMYOPATHY
Author(s) -
Bolte Craig Steven,
Newman Gilbert,
Schultz Jo El
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a251-a
Subject(s) - opioidergic , stimulation , medicine , dilated cardiomyopathy , opioid receptor , heart failure , opioid , cardiomyopathy , endocrinology , receptor , endogenous opioid , cardiology , (+) naloxone
Opioidergic signaling has recently been determined to negatively regulate cardiac function. Opioid receptor signaling has also been shown to be cardioprotective against ischemia‐reperfusion injury. However, whether this signaling is altered in cardiac pathology is unknown. Using a hamster model of dilated cardiomyopathy (Bio14.6) and the appropriate controls (F1B), we investigated alterations in levels of endogenous opioid peptides, as well as functional changes using the perfused, work‐performing heart setup. We saw no differences in opioid peptide levels at any stage of pathology. However, we observed an altered response to kappa and delta opioid receptor stimulation at different stages of pathology. Delta receptor stimulation caused a significantly more robust response in Bio14.6 than F1B hamsters at 1 month, prior to pathology, however there was no difference in the response at later, pathological, time points. Kappa receptor stimulation was similar at pre‐ and early‐pathology time points but was significantly more efficacious and potent in Bio14.6 at the heart failure time point. That opioidergic stimulation is altered at multiple time points during the progression to heart failure suggests it may be a critical component of the failing heart phenotype.