Central and peripheral roles of prostaglandins in pain and their interactions with novel neuropeptides nociceptin and nocistatin

Ito, Seiji; Okuda‐Ashitaka, Emiko; Minami, Toshiaki

doi:10.1016/s0168-0102(01)00289-9

Cited by 186 publications

(125 citation statements)

References 208 publications

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“…Drugs show significant effect on a viscero somatic model (tonic pain) reflected in a significant reduction of the acetic acid induced abdominal writhes. The abdominal writhing induced by acetic acid involves the production and release of arachidonic acid metabolite via cyclooxygenase (COX) and PG biosynthesis (Ferreira et al, 1979;Elisabetsky et al, 1995;Ito et al, 2001). Activation of AT 1 receptor with Ang II also increases Ca influx; therefore, blockage may possesed analgesic activity.…”

Section: Discussionmentioning

confidence: 99%

Analgesic activity of angiotensin antagonists

Indumathy¹

2011

Afr. J. Pharm. Pharmacol.

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Angiotensin Receptor Antagonists (ARAs) are widely used compounds in various cardiovascular disorders like Hypertension, Stroke prophylaxis, Heart failure. In addition, they are approved for the treatment of Diabetic Nephropathy. It is reported to produce analgesia on intracerebro-ventricular administration that could be blocked by naloxone. Angiotensin II has been reported for its pronociceptive activity. Angiotensin receptor antagonists block the action of angiotensin II by inhibiting its binding with its receptor hence, they exerts analgesic activity. The analgesic activity of angiotensin antagonists Losartan, Irbesartan and Valsartan evaluated by tail immersion, tail flick and tail clip methods have shown significant increase in basal reaction time. Pentazocine, a kappa receptor agonist exerted a significant analgesic effect (p<0.001). In comparison to control, angiotensin antagonists Losartan, Irbesartan and Valsartan show significant reduction in time for onset of writhing and also number of writhing. The % inhibitions of writhing for Losartan, Irbesartan and Valsartan at a dose of 20 mg/kg were 74, 68 and 73% respectively, whereas Aspirin (100 mg/kg) has 83% inhibition. All the three drugs have shown significant p value (p<0.001) which is comparable to standard control

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Section: Discussionmentioning

confidence: 99%

Analgesic activity of angiotensin antagonists

Indumathy¹

2011

Afr. J. Pharm. Pharmacol.

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“…35,41 It appears that COX-2 has an important role in healing damaged mucosa in the GI tract, and although COX-2 has been shown to be constitutively expressed in the canine GI tract, 42,43 information on cats is lacking. While COX-1 is the predominant constitutively produced enzyme, COX-2 is predominantly inducible and its production is dramatically upregulated during inflammation, in which it plays a central role.…”

Section: Expression Of Cox Enzymesmentioning

confidence: 99%

ISFM and AAFP Consensus Guidelines: Long-Term use of NSAIDs in Cats

Sparkes

Heiene

Lascelles

et al. 2010

Journal of Feline Medicine and Surgery

104

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NSAIDs and cats Non-steroidal anti-inflammatory drugs (NSAIDs) are an important class of drug in feline medicine, having analgesic, anti-inflammatory and antipyretic activity. While most published data on their use in this species relate to short-term (often perioperative) therapy, there is increasing evidence of the value of these drugs in treating chronic pain in cats (for example, that associated with degenerative joint disease), and some NSAIDs have now become licensed for long-term use in cats in some geographies. Most of our knowledge of therapeutic mechanisms or adverse drug reactions associated with NSAIDs is extrapolated from work in other species, and there is a paucity of published data relating to cats. Guidelines These guidelines have been drawn together by an expert panel, which have reviewed the current literature on long-term NSAID use in cats and other species, and developed guidance on their use based on this information. The aim is to provide practical information for veterinarians to encourage appropriate NSAID therapy whenever cats will benefit from the use of these drugs.

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“…We have demonstrated that many substances involved in spinal synaptic transmission, such as PGE 2 , PGF 2a , NMDA, AMPA, and NO, could induce allodynia when injected intrathecally (Eguchi et al, 1999;Ito et al, 2001). We previously showed that the allodynia induced by i.t.…”

Section: T Minami Et Almentioning

confidence: 99%

“…kainate could not evoke allodynic responses at all . In contrast to extensive studies on mechanisms of induction and maintenance of pain by spinal NMDA receptors (Meller & Gebhart, 1993;Ito et al, 2001), studies on those by non-NMDA receptors are limited. Although ACRO can be a cause of prominent allodynic responses that last for a month following ingestion of the poisonous mushroom, the involvement of ACRO in induction of allodynia and its relation to the excitotoxicity remain to be clarified.…”

Section: Introductionmentioning

confidence: 99%

Acute and late effects on induction of allodynia by acromelic acid, a mushroom poison related structurally to kainic acid

Minami

Matsumura

Nishizawa

et al. 2004

British J Pharmacology

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1 Ingestion of a poisonous mushroom Clitocybe acromelalga is known to cause severe tactile pain (allodynia) in the extremities for a month and acromelic acid (ACRO), a kainate analogue isolated from the mushroom, produces selective damage of interneurons of the rat lower spinal cord when injected either systemically or intrathecally. Since ACRO has two isomers, ACRO-A and ACRO-B, here we examined their acute and late effects on induction of allodynia. 2 Intrathecal administration of ACRO-A and ACRO-B provoked marked allodynia by the first stimulus 5 min after injection, which lasted over the 50-min experimental period. Dose-dependency of the acute effect of ACRO-A on induction of allodynia showed a bell-shaped pattern from 50 ag kg À1 to 0.5 pg kg À1 and the maximum effect was observed at 50 fg kg À1 . On the other hand, ACRO-B induced allodynia in a dose-dependent manner from 50 pg kg À1 to 50 ng kg ). Higher doses of ACRO-A, however, could evoke allodynia dose-dependently from 50 pg kg À1 to 500 ng kg À1 in the ACRO-A-treated mice. The allodynia induced by ACRO-A (500 ng kg À1 ) was not inhibited by Joro spider toxin or NMDA receptor antagonists. These properties of the late allodynia induced by ACRO-A were quite similar to those of the acute allodynia induced by ACRO-B. 5 ACRO-A could increase [Ca 2 þ ] i in the deeper laminae, rather than in the superficial laminae, of the spinal cord. This increase was not blocked by the AMPA-preferring antagonist GYKI52466 and Joro spider toxin. 6 Taken together, these results demonstrate the stereospecificity of ACRO for the induction of allodynia and suggest the presence of a receptor specific to ACRO.

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Central and peripheral roles of prostaglandins in pain and their interactions with novel neuropeptides nociceptin and nocistatin

Cited by 186 publications

References 208 publications

Analgesic activity of angiotensin antagonists

Analgesic activity of angiotensin antagonists

ISFM and AAFP Consensus Guidelines: Long-Term use of NSAIDs in Cats

Acute and late effects on induction of allodynia by acromelic acid, a mushroom poison related structurally to kainic acid

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