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Opioid receptor activation alters beta‐adrenergic receptor function in heart failure
Author(s) -
Schultz Jo El Jean,
Natter Amanda B,
Dunn Caitlin,
Bolte Craig S
Publication year - 2012
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.26.1_supplement.1123.4
Subject(s) - contractility , medicine , stimulation , endocrinology , propranolol , receptor , heart failure , adrenergic receptor , κ opioid receptor , opioid receptor , dobutamine , opioid , chemistry , hemodynamics
Our lab previously demonstrated that opioid receptor (OR) stimulation significantly enhanced the decreased cardiac function in animal models predisposed to or with heart failure (HF). Opioid and beta receptors have opposing effects in the healthy heart, such that OR stimulation decreases and beta receptor signaling increases cardiac function. Yet, the interaction between the two receptors during HF is unknown. To investigate this, hearts from a hamster model predisposed to or with HF and their controls will be subjected to simultaneous agonism of opioid and β 1 ‐adrenergic receptors. Dobutamine (DOB) increased contractility in 1 month hamster hearts which was blocked by propranolol; whereas, diminished beta‐adrenergic effect on contractility in 8 month failing heart was observed compared to the wildtype (p<0.05). A similar decrease in DOB‐induced contractility was seen in 1 month hearts upon kappa or delta OR activation. Failing hearts had a lesser decrease (20%) in DOB‐induced contractility upon kappa OR stimulation compared to wildtype (40%, p<0.05). Conversely, upon delta OR agonism, failing hearts had a significant decrease (81%) in DOB‐induced contractility compared to wildtype (28%, p<0.05). In conclusion, OR activation modulates beta‐adrenergic receptor function in HF and will provide a better understanding of these receptors as they pertain to HF treatment. Research funded by NIH/NIDA R21 DA0804.