Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effect of opioids on the heat stimulus-evoked release of substance P (SP) into the subcutaneous space and the formation of edema in the rat hind paw. Immersion of the rat hind paw for 30 min into hot water adjusted to 47 degrees C led to a marked increase in the release of SP into the subcutaneous perfusate with the formation of thermal edema. Intra-arterial infusion of morphine (10-100 mumol/kg) or ethylketocyclazocine (30-100 mumol/kg) inhibited dose dependently the heat stimulus-evoked increase in SP release and the thermal edema and the inhibitory effects were antagonized by pretreatment with N-methyl levallorphan (10 mg/kg i.p.) and Win 44,441-3 (10 mg/kg i.p.). The heat stimulus-evoked release of SP was reduced significantly during the intra-arterial infusion of [D-Ala2,Met5] enkephalinamide (100 mumol/kg). These results suggest that the opioid-induced inhibition of heat-induced edema could result from inhibition of the release of SP from peripheral sensory nerve endings.
 ...
PMID:Effects of opioids on the heat stimulus-evoked substance P release and thermal edema in the rat hind paw. 246 24

Nootropic non-anticholinesterase organophosphorus preparation CAPAH and substance P produced similar and dose-dependent effects on the amplitude and temporal parameters of miniature endplate potentials in mammalian neuromuscular synapse. Neurokinin receptor antagonist Win-51.708 abolished the effects of these agents. In behavioral experiments substance P moderated the mnemotropic and antidepressant effects of CAPAH. It was assumed that neurokinin receptors are the targets of CAPAH and substance P in CNS and neuromuscular synapse.
 ...
PMID:Possible involvement of neurokinin receptors in CNS and neuromuscular synapse in the realization of the effects of CAPAH and substance P. 1251 99

To investigate the role of substance P (sP), nitric oxide (ON) and prostaglandins (PGs) in acrolein (ACR)-induced cystitis, we studied the changes induced by ACR on bladder inducible nitric oxide synthase (iNOS) and mieloperoxidase (MPO) activities, along with PGs and NO metabolites levels. Sprague-Dawley male rats received i.p. ACR (5 mg/Kg) plus one of the following treatments: Group 1: saline 0.10 mL/100g i.p.; Group 2: Win-51.708 (WIN) 25 mg/Kg i.p.; Group 3: S-metilisothiourea (MITU) 35 mg/Kg i.p.; Group 4: Rofecoxib(ROF) 20 mg/Kg o.p.; Group 5: Meloxicam(MEL) 25 mg/Kg i.p.; Group 6: combination MITU+MEL. ACR-induced mortality was partially prevented by WIN (NK1 antagonist) and MITU (iNOS inhibitor). Animals that survived after 24h of ACR exposure, had histological inflammatory changes in bladder along with increased MPO activity. There was augmentation of nitrates+nitrites and of PGs. WIN didn't prevent any of these effects. ROF and MEL (COX-2 inhibitors) partially protected against bladder inflammation; MITU pre-treatment was able to prevent these changes and those of NO metabolites levels. The MITU+MEL combination produced the highest protection against ACR-induced damage. These results suggest that NO produced via iNOS and PGs produced by COX-1/COX-2, have an important role in the pathogenesis of cystitis induced by ACR. ACR could stimulate iNOS and COX-1/COX-2, producing lymphocyte migration and increases of NO and PGs.
 ...
PMID:[Changes in nitric oxide, prostaglandins and myeloperoxidase activity in acrolein-induced cystitis in rats]. 1941 24