Antinociceptive effects of Ca2+ channel blockers

Miranda, Hugo F.; Bustamante, Diego; Krämer, Verónica; Pélissier, Teresa; Saavedra, H.; Paeile, C.; Fernández, E; Pinardi, G.

doi:10.1016/0014-2999(92)90833-p

Cited by 104 publications

(41 citation statements)

References 23 publications

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“…These studies indicate that brief, phasic nociceptive tests, such as the tail-flick and hot-plate tests, are unaffected by Ca 2 + (Harris et al 1975;Chapman and Way 1982), Ca2+ chelators (Harris et al 1975;Ben-Sreti et al 1983), or Ca2+ channel antagonists (Benedek and Sikszay 1984;Contreras et al 1988), while tonic nociceptive tests, such as the formalin and acetic acid-induced writhing tests, are sensitive to Ca 2 +, Ca2+ ionophores and Ca 2 + channel agonists (Chapman and Way 1982;Coderre and Melzack 1992b) which increase nociceptive responses, or Ca 2 + chelators and Ca 2 + channel antagonists (Del Pozo et al 1987;Coderre and Melzack 1992b;Miranda et al 1992) which reduce nociceptive responses.…”

Section: Intracellular Calciummentioning

confidence: 99%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,823

700

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SummaryPeripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also playa significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (eNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in eNS function which influence subsequent pain experience.

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Section: Intracellular Calciummentioning

confidence: 99%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,823

700

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“…Furthermore, bisphosphonates have a central antinociceptive effect connected with the Ca 2ϩ mechanism. Ca influx releases substances involved in nociception and inflammation, such as substance P, vasoactive intestinal peptide, neuropeptide Y, prostaglandin, serotonin, and kinines (17)(18)(19). We did not detect the initial fall of the temperature linked to the bisphosphonates because we checked it at the beginning and end of the study (20).…”

Section: Research Design Andmentioning

confidence: 99%

Six-Month Treatment With Alendronate in Acute Charcot Neuroarthropathy

et al. 2005

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“…Further, Xu et al (1992b) (Yamamoto & Yaksh, 1991;Nagahisa et al, 1992a). Several (Miranda et al, 1992), the detection of non-specific activity of CP-96,345 at ion channels (Schmidt et al, 1992) and the report that the antinociceptive effects of CP-96,345 in several behavioural tests in the rat is not enantioselective (Nagahisa et al, 1992b (Garret et al, 1991;Nagahisa et al, 1992a;Lembeck et al, 1992;Shepheard et al, 1993). Thus the evidence for anti-nociceptive activity of NK, receptor antagonists in behavioural tests is equivocal.…”

Section: Pharmacokineticsmentioning

confidence: 99%

Effect of RP 67580, a non‐peptide neurokinin₁ receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat

Laird¹,

Hargreaves²,

Hill³

1993

British J Pharmacology

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1 In order to examine the contribution of neurokinin, (NKI) receptors to facilitation of a spinal nociceptive reflex in the rat, we have investigated the effects of RP 67580 ((3aR,7aR)-7,7-diphenyl-2(1-imino-2-(2-methoxyphenyl/ethyl)perhydroisoindole)), a non-peptide neurokinin, (NK,) receptor antagonist, selective for the rodent receptor sub-type, on the activity of individual motorunits. These results were compared with the effects of RP 68651, the inactive 3aS, 7aS enantiomer of RP 67580, as a control for non-specific activity. 2 Experiments were performed on 15 rats anaesthetized with a continuous i.v. infusion of alphaxalone/ alphadalone and spinalized at T9-10. Single unit recordings of motorunit activity from biceps femoris/ semitendinosus were made with a concentric needle electrode. In each experiment, a vehicle dose followed by 4 sequential rising doses of either RP 67580 or RP 68651 were given at 15 min intervals. High intensity electrical stimuli were applied to the hindlimb receptive field of the motorunit at a rate of 1 per 60 s throughout the experiment to establish a baseline. A conditioning stimulus (20 of these stimuli at 1 Hz) was delivered 5 min after each dose and the effect of the size of the baseline response examined. 3 The conditioning stimulus evoked a facilitation of the baseline at the start of all experiments (mean increase ± s.e.mean = 151 ± 20%). RP 67580 attenuated this facilitation, with an IDso (± s.e.mean) of 2.5 ± 4.2 fg kg-', i.v., whereas RP 68651 at doses of up to 3 mg kg', i.v. did not. There was no statistically significant effect of drug on the baseline reflex, nor on the response to the conditioning stimulus. Doses of 300 and 3000 Itg kg-' of both RP 67580 and RP 68651 evoked small depressor effects on systemic arterial blood pressure. 4 We conclude that the facilitation of a spinal flexor reflex by noxious conditioning stimuli in the rat is mediated by NK, receptors whereas the baseline reflex is not. The results suggest that brain penetrant NK, receptor antagonists may have central anti-nociceptive effects.

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Antinociceptive effects of Ca2+ channel blockers

Cited by 104 publications

References 23 publications

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Six-Month Treatment With Alendronate in Acute Charcot Neuroarthropathy

Effect of RP 67580, a non‐peptide neurokinin₁ receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat

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Antinociceptive effects of Ca2+ channel blockers

Cited by 104 publications

References 23 publications

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Six-Month Treatment With Alendronate in Acute Charcot Neuroarthropathy

Effect of RP 67580, a non‐peptide neurokinin1 receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat

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Effect of RP 67580, a non‐peptide neurokinin₁ receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat