Potentiation of morphine analgesia by BQ123, an endothelin antagonist

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

doi:10.1016/s0196-9781(02)00141-9

Cited by 31 publications

(22 citation statements)

References 23 publications

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“…We have previously reported that BQ123 does not affect [ 3 H]-naloxone binding in normal rats [24]. The results of the present study show that there is no change in binding to ET receptors in the brain of morphine-tolerant neonatal rats.…”

Section: Discussionsupporting

confidence: 46%

“…ET antagonists have also been shown to block sympathetic nervous systemmediated responses of clonidine and propranolol [32,33]. We provide evidence that intracerebroventricular admin-istration of an ET A receptor antagonist, BQ123, significantly potentiates the morphine-induced analgesic response in adult rats [24]. We have also demonstrated that BQ123 and BMS182874 restore the analgesic effect of morphine and potentiate morphine-induced analgesia in morphine-tolerant adult rats [34].…”

Section: Discussionmentioning

confidence: 61%

“…We have reported that the ET A receptor antagonist, BQ123, significantly potentiated the analgesic and hyperthermic responses induced by morphine, without affecting morphine-induced catalepsy [24]. It is clear that there is a functional interaction between ET and opiates, but the mechanism is not known.…”

Section: Introductionmentioning

confidence: 97%

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Evidence that Morphine Tolerance May Be Regulated by Endothelin in the Neonatal Rat

Puppala

Matwyshyn²,

Bhalla³

et al. 2004

Neonatology

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Section: Discussionsupporting

confidence: 46%

Section: Discussionmentioning

confidence: 61%

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Evidence that Morphine Tolerance May Be Regulated by Endothelin in the Neonatal Rat

Puppala

Matwyshyn²,

Bhalla³

et al. 2004

Neonatology

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“…It is possible that the elapsed time since injection was insufficient for the emergence of hypothermia [6].…”

Section: Catalepsy Body Temperature and Antinociception Studymentioning

confidence: 99%

Stress-opioid interactions: a comparison of morphine and methadone

Taracha

Mierzejewski

Lehner

et al. 2009

Pharmacological Reports

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Abstract:The utility of methadone and morphine for analgesia and of methadone for substitution therapy for heroin addiction is a consequence of these drugs acting as opioid receptor agonists. We compared the cataleptogenic and antinociceptive effects of single subcutaneous doses of methadone hydrochloride (1-4 mg/kg) and morphine sulfate (2.5-10 mg/kg) using catalepsy and hot-plate tests, and examined the effects of the highest doses of the drugs on Fos protein expression in selected brain regions in male Sprague-Dawley rats. Methadone had greater cataleptogenic and analgesic potency than morphine. Fos immunohistochemistry revealed substantial effects on the Fos response of both the stress induced by the experimental procedures and of the drug exposure itself. There were three response patterns identified: 1) drug exposure, but not stress, significantly elevated Fos-positive cell counts in the caudate-putamen; 2) stress alone and stress combined with drug exposure similarly elevated Fos-positive cell counts in the nucleus accumbens and cingulate cortex; and 3) methadone and morphine (to a lesser extent) counteracted the stimulatory effect of nonpharmacological stressors on Fos protein expression in the somatosensory cortex barrel field, and Fos-positive cell counts in this region correlated negatively with both the duration of catalepsy and the latency time in the hot-plate test. The overlap between brain regions reacting to nonpharmacological stressors and those responding to exogenous opioids suggests that stress contributes to opioid-induced neuronal activation.

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“…The mechanism of interaction between opiate and nonopiate systems has been investigated, and non-opiate systems such as nitric oxide, N-methyl-D-aspartate, Á-aminobutyric acid, dopamine, adrenergic, 5-hydroxytryptamine, cholecystokinin, adenosine, and glutamate have been proposed to take part in the mechanism of action of opiates [3,4]. Studies from our laboratory have shown that endothelin A (ET A ) receptor antagonists enhance the analgesic effect of morphine [5].…”

Section: Introductionmentioning

confidence: 99%

Central Endothelin-B Receptor Stimulation Does Not Affect Morphine Analgesia in Rats

Bhalla¹,

Matwyshyn²,

Gulati

2004

Pharmacology

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Several neurotransmitter mechanisms have been proposed to play a role in the actions of morphine. We reported that centrally administered endothelin A (ET_A) receptor antagonists potentiate morphine analgesia in rats. It has also been reported that ET_B agonist, IRL1620, has antinociceptive action mediated through opiate receptors in the periphery. The present study was conducted to determine if central ET_B receptors are involved in analgesic actions of morphine. The effect of intracerebroventricular (i.c.v.) administration of ET_B receptor agonist, IRL1620, on morphine-induced analgesia and hyperthermia was determined in the rat. Morphine (4 mg/kg, s.c.) produced a significant increase (84%) in tail-flick latency compared to the control group and the analgesic response lasted for 4 h. IRL1620 (30 µg, i.c.v.) did not produce any increase (16%) in tail-flick latency over the 5-hour observation period in vehicle-treated rats. Pretreatment with IRL1620 (3, 10, and 30 µg, i.c.v.) did not have any significant effect on the intensity and duration of morphine (4 mg/kg, s.c.)-induced analgesia. Morphine (4 mg/kg, s.c.) administration produced an increase in body temperature compared to the control group. In vehicle-pretreated rats, IRL1620 (30 µg, i.c.v.) did not produce any change in body temperature. The morphine-induced hyperthermic effect was not altered in IRL1620-pretreated rats. These studies demonstrate that IRL1620, a specific ET_B receptor agonist, did not affect the morphine-induced analgesic and hyperthermic effect in rats. It can be concluded that central ET_B receptors are not involved in modulation of pharmacological actions of morphine.

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Potentiation of morphine analgesia by BQ123, an endothelin antagonist

Cited by 31 publications

References 23 publications

Evidence that Morphine Tolerance May Be Regulated by Endothelin in the Neonatal Rat

Evidence that Morphine Tolerance May Be Regulated by Endothelin in the Neonatal Rat

Stress-opioid interactions: a comparison of morphine and methadone

Central Endothelin-B Receptor Stimulation Does Not Affect Morphine Analgesia in Rats

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