Morphine tolerance does not develop in mice treated with endothelin-A receptor antagonists

Bhalla, Shaifali; Matwyshyn, George A.; Gulati, Anil

doi:10.1016/j.brainres.2005.09.054

Cited by 23 publications

(19 citation statements)

References 54 publications

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“…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: 98%

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: Introductionmentioning

confidence: 98%

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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“…Further, endothelin ET A antagonists prevented or reversed tolerance to morphine analgesia [33,44,45] . We have shown that the endothelin ET A receptor antagonists sulfisoxazole [17] and BMS182874 potentiate the analgesic effects of clonidine in mice [10] and that these actions are mediated through the imidazoline and opioid receptors.…”

Section: Discussionmentioning

confidence: 92%

“…It has been shown that endothelin ET A receptor antagonists potentiate morphine analgesia in rodents [33,42,43] without potentiating its side effects [43] . Further, endothelin ET A antagonists prevented or reversed tolerance to morphine analgesia [33,44,45] .…”

Section: Discussionmentioning

confidence: 99%

“…BQ123 [cyclo( D -Trp-D -Asp-Pro-D -Val-Leu); Tocris Bioscience, Ellisville, Mo., USA] was dissolved in sterile saline and was injected intracerebroventricularly (1, 3, 9 g i.c.v.). Doses of BQ123 were selected based on previous studies [33] . Sulfisoxazole (Sigma Chemical Company) was dissolved in carboxymethyl cellulose and was administered orally (25,75 and 225 mg/kg p.o.).…”

Section: Drugs and Chemicalsmentioning

confidence: 99%

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Assessment of the Analgesic Effect of Centhaquin in Mouse Tail Flick and Hot-Plate Tests

Andurkar

Gulati²

2011

Pharmacology

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Background: Centhaquin is a centrally acting hypotensive drug like clonidine. Clonidine also produces analgesia and hypothermia in mice and potentiates morphine analgesia. Clonidine analgesia is blocked by idazoxan and naloxone while it is potentiated by BQ123 and sulfisoxazole. This study was conducted to determine the analgesic and hypothermic properties of centhaquin, and to assess whether it potentiates morphine analgesia. Yohimbine (α₂-adrenergic antagonist), idazoxan (imidazoline/α₂-adrenergic antagonist), naloxone (opioid antagonist), and BQ123 and sulfisoxazole (endothelin ET_A antagonists) were used to study the involvement of these receptors in centhaquin analgesia and hypothermia. Methods: Analgesic (tail flick and hot-plate tests) latencies and body temperatures were measured in male Swiss Webster mice treated with vehicle plus centhaquin, antagonists plus centhaquin or centhaquin plus morphine. Results: Centhaquin produced dose-dependent analgesia which was partially blocked by yohimbine, idazoxan and naloxone. BQ123 and sulfisoxazole did not affect centhaquin analgesia. Morphine analgesia was not potentiated by centhaquin. Centhaquin produced mild hypothermia which was not blocked by yohimbine, idazoxan, naloxone, BQ123 or sulfisoxazole. Conclusions: This is the first report demonstrating the analgesic activity of centhaquin. The α₂-adrenergic, imidazoline and opioid receptors are involved in mediating centhaquin analgesia. Endothelin ET_A receptors do not play a role in centhaquin analgesia; centhaquin does not augment morphine analgesia.

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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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Morphine tolerance does not develop in mice treated with endothelin-A receptor antagonists

Cited by 23 publications

References 54 publications

Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Endothelin ET_Areceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Assessment of the Analgesic Effect of Centhaquin in Mouse Tail Flick and Hot-Plate Tests

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

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Morphine tolerance does not develop in mice treated with endothelin-A receptor antagonists

Cited by 23 publications

References 54 publications

Endothelin ETAreceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Endothelin ETAreceptor antagonist reverses naloxone-precipitated opioid withdrawal in mice

Assessment of the Analgesic Effect of Centhaquin in Mouse Tail Flick and Hot-Plate Tests

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

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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