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

Basal as well as agonist (100 microM substance P or 2 mM carbachol)-stimulated phosphatidylinositol hydrolysis was investigated in slices of rat spinal cord and cerebral cortex, in the presence and absence of pentobarbital (5-50 microM in vitro or 65 mg/kg in vivo) or urethane (0.2 mM in vitro or 1.4 g/kg in vivo). Urethane was without effect; pentobarbital, however, inhibited the basal hydrolysis and the agonist-stimulated phosphatidylinositol hydrolysis (in dose-dependent fashion in vitro). It is suggested that inhibition of phosphatidylinositol hydrolysis may be part of the cellular mechanisms by which pentobarbital produces anaesthesia.
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PMID:Anaesthetic doses of pentobarbital antagonize phosphatidylinositol hydrolysis induced by substance P or carbachol in the spinal cord and cerebral cortex of the rat. 138 86

Urethane and ketamine were tested for their ability to alter the caudally directed binding and scratching response elicited by the intrathecal (i.t.) injection of excitatory amino acids (EAAs) or substance P (SP). EAAs, such as N-methyl-D-aspartate (NMDA), kainate acid and quisqualic acid, but not SP, were inhibited by subanesthetic doses of urethane. In contrast, SP was more sensitive than NMDA to the inhibitory effect of (+)-ketamine. (-)-Ketamine produced much less inhibition of the SP-induced behaviors than the (+)isomer. These results have important implications regarding the use of urethane and ketamine as anesthetics for studies in which these excitatory compounds are potential mediators.
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PMID:Effects of urethane and ketamine on substance P- and excitatory amino acid-induced behavior in mice. 169 43

Urethane (50 mM) produced a non-selective antagonism of depolarizations evoked by excitant amino acids or carbachol recorded from ventral roots of isolated spinal cord preparations of the frog or immature rat. Depolarizing responses to substance P or eledoisin-related-peptide were either unaffected or potentiated by this concentration of urethane. The threshold level for depression of dorsal to ventral root transmission was 10 mM urethane and transmission was completely blocked at 70-100 mM urethane. It is suggested that post-junctional blockade of the actions of excitant amino acids may be important in the anaesthetic action of urethane.
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PMID:Effect of urethane on synaptic and amino acid-induced excitation in isolated spinal cord preparations. 612 91

Prolonged or repetitive bouts of hypoxia may desensitize the brain stem respiratory centres leading to reduced stimulation of ventilation. We investigated the possible involvement of changes in the sensitivity of the commissural nucleus of the solitary tract (cNTS) to the tachykinin peptide, substance P (SP). Urethane-anaesthetised rats were allowed to breath room air (normoxic) or subjected to four, 30 s bouts of hypoxia (10% O2/90% N2) prior to the injection of SP (750 pmol) into the cNTS. In normoxic rats (n = 5), SP produced a fall in frequency (f, 88+/-4% control) after 4 min and a maximum rise in tidal volume (VT) after 6 min (138+/-10% control) leading to an overall increase in minute ventilation (VE, maximum, 127+/-12% control after 2 min). In rats (n = 5) exposed to four bouts of hypoxia and allowed to recover for 10 min, injection of SP produced a similar fall in f but a delayed and significantly (P < 0.001) reduced VT (maximum after 10 min, 110+/-1% control) and hence, VE response (104+/-3% control). Sixty min after hypoxia, the f, VT and VE responses to SP were identical to those of normoxic rats. These data suggest that hypoxia desensitizes SP receptors in the cNTS and this may partly explain why the respiratory response to hypoxia declines over time.
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PMID:Hypoxia attenuates the respiratory response to injection of substance P into the nucleus of the solitary tract of the rat. 983 4