Effect of endothelin-A receptor antagonist on mu, delta and kappa opioid receptor-mediated antinociception in mice

Bhalla, Shaifali; Zhang, Zhong; Patterson, Nicole; Gulati, Anil

doi:10.1016/j.ejphar.2010.03.003

Cited by 18 publications

(19 citation statements)

References 45 publications

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“…It has also been demonstrated that ET A receptor antagonists eliminate analgesic tolerance in mice and rats (Bhalla et al 2003(Bhalla et al , 2005Bhalla et al 2010). Since ET A receptors play an important role in acute opioid analgesia and tolerance to various opioids, it is possible that these receptors may also be involved in opioid withdrawal.…”

Section: Discussionmentioning

confidence: 96%

“…Tolerance to opioid agonists was induced using a 3-day (Ozdogan et al 2003) and 5-day (Bhalla et al 2010) cumulative dosing regimen for morphine and oxycodone, respectively.…”

Section: Induction Of Tolerance and Precipitation Of Opioid Withdrawalmentioning

confidence: 99%

“…Treatment with ET A receptor antagonist, BQ123, significantly potentiated morphine analgesia in mice and rats (Bhalla et al 2002(Bhalla et al , 2005. It was demonstrated that morphine and oxycodone tolerance in mice and rats can be eliminated by ET A receptor antagonists, BQ123 and BMS182874 (Bhalla et al 2003(Bhalla et al , 2005Bhalla et al 2010). Our previous studies have shown that ET B receptors are not involved in opioid analgesia (Bhalla et al 2004).…”

Section: Introductionmentioning

confidence: 96%

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Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Bhalla

Pais

Tapia

et al. 2015

Can. J. Physiol. Pharmacol.

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Long-term use of opioids for pain management results in rapid development of tolerance and dependence leading to severe withdrawal symptoms. We have previously demonstrated that endothelin-A (ETA) receptor antagonists potentiate opioid analgesia and eliminate analgesic tolerance. This study was designed to investigate the involvement of central ET mechanisms in opioid withdrawal. The effect of intracerebroventricular administration of ETA receptor antagonist BQ123 on morphine and oxycodone withdrawal was determined in male Swiss Webster mice. Opioid tolerance was induced and withdrawal was precipitated by the opioid antagonist naloxone. Expression of ETA and ETB receptors, nerve growth factor (NGF), and vascular endothelial growth factor was determined in the brain using Western blotting. BQ123 pretreatment reversed hypothermia and weight loss during withdrawal. BQ123 also reduced wet shakes, rearing behavior, and jumping behavior. No changes in expression of vascular endothelial growth factor, ETA receptors, and ETB receptors were observed during withdrawal. NGF expression was unaffected in morphine withdrawal but significantly decreased during oxycodone withdrawal. A decrease in NGF expression in oxycodone- but not in morphine-treated mice could be due to mechanistic differences in oxycodone and morphine. It is concluded that ETA receptor antagonists attenuate opioid-induced withdrawal symptoms.

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Section: Discussionmentioning

confidence: 96%

“…Tolerance to opioid agonists was induced using a 3-day (Ozdogan et al 2003) and 5-day (Bhalla et al 2010) cumulative dosing regimen for morphine and oxycodone, respectively.…”

Section: Induction Of Tolerance and Precipitation Of Opioid Withdrawalmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Bhalla

Pais

Tapia

et al. 2015

Can. J. Physiol. Pharmacol.

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“…The analgesic effects of opioid agonists, morphine, and oxycodone are potentiated by the ET A receptor antagonist BMS182874, suggesting a functional interaction between opioid receptors and ET A receptors [1,3,49] . Potentiation of morphine and oxycodone analgesia has also been demonstrated with clonidine, an ␣ 2 -adrenergic and imidazoline receptor agonist, indicating a functional interaction of opioid receptors with ␣ 2 -adrenergic and imidazoline receptors [28,31,50] .…”

Section: Discussionmentioning

confidence: 99%

Study of Adrenergic, Imidazoline, and Endothelin Receptors in Clonidine-, Morphine-, and Oxycodone-Induced Changes in Rat Body Temperature

Bhalla¹,

Andurkar²,

Gulati³

2011

Pharmacology

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Objectives: The potentiation of morphine or oxycodone analgesia by endothelin-A (ET_A) receptor antagonists and imidazoline/α₂-adrenergic agonists is well documented. However, the effect of morphine or oxycodone in combination with an ET_A receptor antagonist or an imidazoline/α₂ adrenergic agonist on body temperature is not known. The present study was carried out to study the role of ET_A and imidazoline/α₂ adrenergic receptors in body temperature effects of morphine, oxycodone, and clonidine in rats. Methods: Body temperature was determined in male Sprague-Dawley rats treated with morphine, oxycodone, or clonidine. Yohimbine, idazoxan, and BMS182874 were used to determine the involvement of α₂-adrenergic, imidazoline, and ET_A receptors, respectively. Key Findings: Morphine and oxycodone produced hyperthermia which was not affected by α₂-adrenergic antagonist yohimbine, imidazoline/α₂-adrenergic antagonist idazoxan, or ET_A receptor antagonist BMS182874. Clonidine alone produced hypothermia that was comparable to the hypothermia observed with clonidine plus morphine or oxycodone. The hypothermic effect of clonidine was blocked by idazoxan and yohimbine. The blockade by idazoxan was more pronounced compared to yohimbine. Clonidine hypothermia was not affected by BMS182874. Conclusions: This is the first report demonstrating that ET_A receptors do not influence morphine- and oxycodone- induced hyperthermia or clonidine-induced hypothermia. Imidazoline receptors and α₂-adrenergic receptors are involved in clonidine-induced hypothermia, but not in morphine- and oxycodone-induced hyperthermia.

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“…Subsequent studies have demonstrated that ET B receptor induced angiogenesis and neurogenesis occurs, at least in part, via altering expression of VEGF, NGF and PI3K [19, 20]. In previous studies, we have shown that ET A receptor antagonists potentiate morphine analgesia in mice and rats [21, 22] and reverse opioid tolerance via a G-protein mediated mechanism [22, 23, 24]. In an acute study it was found that ET B receptors are not involved in morphine analgesia [25], however, the role of ET B receptors in opioid tolerance has never been investigated.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of opioid tolerance by ET B receptor agonist, IRL-1620, is independent of an accompanied decrease in nerve growth factor in mice

Gulati

Briyal

Jones

et al. 2017

Heliyon

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AimETA receptor antagonists reverse opioid tolerance but the involvement of ETB receptors is unknown. In morphine or oxycodone tolerant mice we investigated (1) the effect of ETB receptor agonist, IRL-1620, on analgesic tolerance; (2) changes in expression of the brain ETA and ETB receptors; and (3) alterations in the brain VEGF, NGF, PI3K and notch-1 expression.Main methodsBody weight, body temperature, and tail-flick latency were assessed before and after a challenge dose of morphine or oxycodone in vehicle or IRL-1620 treated mice. Expression studies were carried out using Western blots.Key findingsTail flick latency to a challenge dose of opioid was significantly increased by IRL-1620 from 39% to 100% in morphine tolerant and from 8% to 83% in oxycodone tolerant mice. Morphine or oxycodone did not alter ETA or ETB receptor expression. IRL-1620 had no effect on ETA however it increased (61%) expression of ETB receptors. IRL-1620-induced increase in ETB receptor expression was attenuated by morphine (39.8%) and oxycodone (51.8%). VEGF expression was not affected by morphine or oxycodone and was unaltered by IRL-1620. However, NGF and PI3K expression was decreased (P < 0.001) by morphine and oxycodone and was unaffected by IRL-1620. Notch-1 expression was not altered by morphine, oxycodone or IRL-1620.SignificanceETB receptor agonist, IRL-1620, restored analgesic tolerance to morphine and oxycodone, but it did not affect morphine and oxycodone induced decrease in NGF/PI3K expression. It is concluded that IRL-1620 attenuates opioid tolerance without the involvement of NGF/PI3K pathway.

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Effect of endothelin-A receptor antagonist on mu, delta and kappa opioid receptor-mediated antinociception in mice

Cited by 18 publications

References 45 publications

Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Study of Adrenergic, Imidazoline, and Endothelin Receptors in Clonidine-, Morphine-, and Oxycodone-Induced Changes in Rat Body Temperature

Attenuation of opioid tolerance by ET B receptor agonist, IRL-1620, is independent of an accompanied decrease in nerve growth factor in mice

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Effect of endothelin-A receptor antagonist on mu, delta and kappa opioid receptor-mediated antinociception in mice

Cited by 18 publications

References 45 publications

Endothelin ETAreceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Endothelin ETAreceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Study of Adrenergic, Imidazoline, and Endothelin Receptors in Clonidine-, Morphine-, and Oxycodone-Induced Changes in Rat Body Temperature

Attenuation of opioid tolerance by ET B receptor agonist, IRL-1620, is independent of an accompanied decrease in nerve growth factor in mice

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Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice