期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 321, 期 4, 页码 C681-C683出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00259.2021
关键词
beta-arrestin; G protein; opioid; respiratory
资金
- National Institutes of Health [R00DA038069, R01DA047978]
- NIH [F31DA053798]
G protein-biased opioid agonists are proposed as safer analgesics with less respiratory depression. Studies have linked respiratory depression to G protein bias and intrinsic efficacy, refuting the role of beta-arrestin signaling in opioid-induced respiratory depression.
Respiratory depression is a potentially fatal side effect of opioid analgesics and a major limitation to their use. G protein-biased opioid agonists have been proposed as safer analgesics with less respiratory depression. These agonists are biased to activate G proteins rather than beta-arrestin signaling. Respiratory depression has been shown to correlate with both G protein bias and intrinsic efficacy, and recent work has refuted the role of beta-arrestin signaling in opioid-induced respiratory depression. In addition, there is substantial evidence that G proteins do, in fact, mediate respiratory depression by actions in respiratory-controlling brainstem neurons. Based on these studies, we provide the perspective that protection from respiratory depression displayed by newly developed G protein-biased agonists is due to factors other than G protein versus arrestin bias.
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