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)

Neurotensin (NT), substance P (SP) and morphine sulfate (MS) elevate plasma prolactin and growth hormone levels in both normal or estrogen-progesterone pretreated male rats. By contrast, steroid priming is required for TRF to exhibit PRL-releasing activity. Naloxone, an opiate receptor blocker, reverses the stimulatory effect of MS only. Diphenhydramine, a histamine antagonist, inhibits the response to NT, SP and MS without affecting the response to TRF. These results suggest the involvement of a histaminic step in the action of NT, SP and MS. TRF, NT and SP do not appear to stimulate PRL and GH through activation of an opiate receptor.
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PMID:Effect of neurotensin, substance P and morphine sulfate on the secretion of prolactin and growth hormone in the rat. 9 1

The pharmacologic actions related to antimotion sickness effects of ginger (Zingiber officinale Roscoe.) were studied. There was no significant effect on parameters of rotatory movement-induced electronystagmogram of rabbit after intravenous (i.v.) infection of ginger juice. The low amplitude fast wave pattern of electrocorticogram of rabbit changed to high amplitude slow wave pattern after i.v. injection of ginger juice. Rabbit gastric contraction in situ was shortly suppressed after ginger juice i.v. administration. In the isolated rat fundus strip preparations, however, ginger juice reduced the spontaneous contractile frequency, and enhanced the spontaneous contractile amplitude, which was followed by inhibition. Ginger juice produced longitudinal contraction of the guinea-pig isolated ileum, which was followed by rapid tachyphylaxis. This contraction effect was not affected by hexamethonium and 5-HT, but could be inhibited by cold storage, hyoscine, morphine, diphenhydramine, promethazine and substance P desensitization. Naloxone could eliminate this inhibition produced by morphine. By using dose-response relationship plot, non-competitive antagonisms were observed between ginger juice and Ach and between ginger juice and histamine in isolated guinea-pig ileum. It is suggested that the pungent constituents of ginger release substance P from sensory fibres. The released substance P in turn either stimulates cholinergic and histaminic neurons to release Ach and histamine, respectively, or produces direct muscle contraction by activating M and H1 receptors correspondingly. It is proposed that after being excited by substance P, M and H1 receptors are inactive temporarily and unable to be excited by agonists, therefore, ginger juice exhibits anticholinergic and antihistaminic action. Ginger juice produces antimotion sickness action possibly by central and peripheral anticholinergic and antihistaminic effects.
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PMID:[Pharmacologic studies of antimotion sickness actions of ginger]. 149 36

Alpha 2-Adrenoceptors mediate analgesia in vivo. The present study explored the actions of the alpha 2-adrenoceptor agonists dexmedetomidine and clonidine on a nociceptive response in isolated neonatal rat spinal cord. Stimulation of a dorsal root generates a slow ventral root potential (slow VRP) at the corresponding ipsilateral ventral root. The slow VRP meets several criteria for a nociceptive response. Dexmedetomidine (10 nM) and clonidine (200 nM) depressed the slow VRP by approximately 80%. Dexmedetomidine's action was approximately linear over the concentration range 0.5-500 nM, whereas clonidine (20 nM-5 microM) exerted biphasic effects. The profile of agonist and antagonist effectiveness characterized the receptor(s) as alpha 2-adrenoceptors; the subtype could not be identified as either alpha 2A or alpha 2B. Naloxone pretreatment partially blocked dexmedetomidine's effect, suggesting a possible endogenous opiate involvement. Dexmedetomidine (0.5-2.0 nM) also depressed the VRP evoked by application of substance P to the cord, implicating postsynaptic as well as possible presynaptic actions. At high concentrations, dexmedetomidine (50-500 nM) depressed the monosynaptic reflex, probably through non-alpha 2-receptor(s). Results from the neonatal spinal cord correlate well with those from in vivo analgesia studies. They suggest an important direct spinal contribution to alpha 2-adrenoceptor-mediated analgesia.
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PMID:Alpha 2-adrenoceptors inhibit a nociceptive response in neonatal rat spinal cord. 167 74

Substance P (SP) found in the dorsal horn of the spinal cord has been proposed as a mediator of nociception. Formalin injected into the hind paw of a rat as a nociceptive stimulus has been shown to increase the amount of immunoreactive SP in the dorsal horn, perhaps by decreasing SP release from primary afferent neurons. These SP changes may be due to the actions of endogenous opiates which can block SP release from primary afferent neurons. In order to determine the time course of SP changes in the dorsal horn and their modulation by naloxone, anesthetized rats pretreated subcutaneously with naloxone or saline were injected in the right hind paw with 0.4 ml of either saline or 5% formalin. After various time intervals, the animals were perfused and the lumbar enlargement of the spinal cord removed. Immunohistochemical staining and manual photometry were used to quantitate SP-like immunoreactivity (SPLI) in the dorsal horn. The results show that saline injection produced an increase in SPLI lasting 20 min, while formalin produced a biphasic effect with early (0-20 min) and late (20-60 min) increases in SPLI. Naloxone pretreatment 30 min prior to hind paw injection partially blocked the initial SPLI increase due to saline or formalin. However, this was not the case if naloxone was injected 2 min following hind paw injection. The formalin-induced late SPLI increase was blocked by naloxone only if it was administered prior to the formalin. This blockade of SPLI increases in the dorsal horn by naloxone implies that endogenous opioid systems play a role in the control of SP levels in the dorsal horn during nociception.
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PMID:Time course of the alteration in dorsal horn substance P levels following formalin: blockade by naloxone. 169 64

The release of gastric substance P-like immunoreactivity (SP-LI) has been studied in the vascularly perfused rat stomach. In the presence of 20 microM bacitracin and captopril, basal release of SP-LI was sustained throughout the experiments. Gastric SP-LI release was stimulated in a concentration-dependent manner by increasing the concentration of KCl in the perfusion medium. This stimulated release was reduced by the omission of Ca2+, indicating that a Ca2(+)-dependent mechanism was involved. Naloxone did not alter basal SP-LI secretion. [Met5]Enkephalin also had no significant effect on K(+)-stimulated secretion suggesting that enkephalinergic mechanisms are not involved. Gastric SP-LI release was also increased by capsaicin perfusion but this was not sustained. In conclusion, the present results provide the first evidence for the release of SP-LI into the rat stomach vasculature.
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PMID:Release of substance P-like immunoreactivity from the vascularly perfused rat stomach. 169 73

In the extrinsically denervated smooth muscle esophagus of the hen anesthetized with urethane (1 g/kg, i. m.), it was studied whether peptidergic neurons in the intramural plexus are involved in the intrinsic reflex. Ascending and descending contractions, and descending relaxation were induced by electrical stimulation of a narrow segment of the esophagus. Naloxone (1 microM), desensitization to substance P (0.3 microM) and spantide (20 microM) inhibited the ascending and descending contractions, respectively. The degree of the inhibition of the contractile response by a combination of naloxone and substance P was nearly the same as that by a single administration of naloxone or substance P. The ascending and descending contractions were reduced to one-third of the control by hexamethonium (100 microM) and abolished by atropine (10 microM). The descending relaxation was abolished after desensitization to vasoactive intestinal peptide (0.3 microM). Taken together the results suggest that in the hen's esophagus, opioid- and substance P-containing neurons in the intramural plexus may act as preganglionic neurons of cholinergic motor neurons in the ascending and descending excitatory pathways and that vasoactive intestinal peptide-containing neurons are involved in the descending inhibitory pathway.
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PMID:Intrinsic reflexes mediated via peptidergic neurons in the smooth muscle esophagus of the hen. 169 22

The functional roles of striatonigral neurokinins were studied by analysing the effects of intranigral injections of substance P and neurokinin A on the extracellular levels of dopamine and dihydroxyphenylacetic acid in the striatum, as measured by in vivo microdialysis in rats. An opioid antagonist, naloxone, and a GABAergic antagonist, bicuculline, were tested and analysed for their ability to modify the neurokinin effects. Unilateral injections of substance P (0.07 nmol) or neurokinin A (0.09 nmol) into the substantia nigra, pars reticulata of halothane anaesthetized rats produced long-lasting increases in ipsilateral striatal dopamine and dihydroxyphenylacetic acid levels. Intranigral injections of naloxone (30 and 300 nmol) produced short-lasting decreases in striatal dopamine, concomitant with an increase in dihydroxyphenylacetic acid. Intranigral injections of 7.0 nmol bicuculline produced an increase, while 70 nmol produced a decrease in striatal dopamine, however, both doses produced an increase in dihydroxyphenylacetic acid. When co-administered intranigrally, the high dose of naloxone (300 nmol) completely blocked the dopamine stimulation of substance P (0.07 nmol), but only moderately inhibited that of neurokinin A (0.09 nmol). The high dose of bicuculline (70 nmol) completely blocked the dopamine stimulation of neurokinin A, but only moderately inhibited that of substance P. Naloxone (30 and 300 nmol) enhanced the dihydroxyphenylacetic acid response to substance P, while bicuculline (70 nmol) inhibited the dihydroxyphenylacetic acid response to neurokinin A. These findings complement and extend the findings in the preceding paper, demonstrating that intranigral substance P and neurokinin A stimulate striatal dopamine via different neuronal mechanisms. We suggest that opioid drugs have a greater influence over substance P while GABAergic drugs have a greater influence over neurokinin A.
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PMID:Effects of intranigral substance P and neurokinin A on striatal dopamine release--II. Interactions with bicuculline and naloxone. 170 Mar 30

Recent evidence suggests that opioids might have excitatory as well as inhibitory actions on neurones. Since substance P (SP) has been implicated in opioid withdrawal, the present experiment was conducted to determine whether SP was released by morphine or morphine withdrawal. Sagittal brain slices and a 2 cm piece of ileum from 5 guinea-pigs were placed in Krebs solution. Morphine 1 microM, produced significant release of SP-like immunoreactivity (SP-LI) within 2 min from brain slices but release from ileum preparations was variable. Naloxone 1 microM, added 5 min after morphine, did not produce significantly greater increase in concentration of SP-LI. It is concluded that morphine releases SP from guinea-pig brain slices.
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PMID:Morphine produces release of substance P-like immunoreactivity from guinea-pig central nervous system. 170 71

Newly developed substance P (SP) analogs with altered N-terminal sequences which equalize the lipophilicity of the N-terminal and C-terminal elements and of their fusion product were examined using i.t. injection in mice. I.t. injection of either the full length analog or the C-terminal hexapeptide (CP) produced biting and scratching behavior similar to that elicited by SP. SPF was approximately 5-fold and CP 14-fold less potent than native SP. The N-terminal peptide (NP) was inactive by itself but inhibited CP-elicited behavior. Naloxone antagonized this action of NP and shifted the SPF dose-response curve 4-fold to the left. However, naloxone had no effect on the action of CP or on the action of any of the native neurokinins. The results are consistent with the hypothesis that N- and C-terminal analogs of SP can have opioid and SP-like actions, respectively, in the CNS of rodents. Furthermore, analogs of SP which include at least the terminal tetrapeptide retain neurokinin activity.
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PMID:Opioid and neurokinin activities of substance P fragments and their analogs. 171 Sep 92

1. The mechanical responses to some autonomic drugs and neuropeptides of longitudinal muscle (LM) and circular muscle (CM) strips isolated from the carp intestinal bulb were investigated in vitro. 2. Acetylcholine and carbamylcholine caused concentration-dependent transient contraction of both LM and CM strips. Tetrodotoxin had no effect, but atropine selectively decreased the contractile responses to acetylcholine and carbamylcholine. 3. Excitatory alpha-2 and inhibitory beta adrenoceptors were present in both LM and CM strips. 4. 5-Hydroxytryptamine (5-HT) caused concentration-dependent contraction of both LM and CM strips. Tetrodotoxin, atropine and methysergide decreased the contractile responses to 5-HT. 5. Some neuropeptides (angiotensin I, angiotensin II, bombesin, bradykinin, neurotensin, somatostatin and vasoactive intestinal polypeptide) did not cause any mechanical response (contraction or relaxation) in either smooth muscle strip. 6. Substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) caused contraction of both LM and CM strips. However, the time course of the contraction in LM was different from that in CM. The order of potency was NKA greater than SP greater than NKB in LM strips and NKA greater than SP much greater than NKB in CM strips. In LM strips, the contractile responses to tachykinins were unaffected by spantide and methysergide, but partly decreased by tetrodotoxin and atropine. On the other hand, the contractile responses of CM strips were unaffected by tetrodotoxin, atropine, methysergide and spantide. 7. Dynorphin (1-13) (DYN), leucine-enkephalin (L-Enk) and methionine-enkephalin (M-Enk) caused concentration-dependent contraction of both LM and CM strips. The order of potency was DYN greater than M-Enk greater than L-Enk. Naloxone selectively decreased the responses to opiate peptides. 8. The present results indicate that acetylcholine, carbamylcholine, catecholamines, 5-HT, tachykinins (SP, NKA and NKB) and opiate peptides (DYN, L-Enk and M-Enk) affect the mechanical activity of LM and CM strips isolated from the carp intestinal bulb through their specific receptors.
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PMID:Effects of some autonomic drugs and neuropeptides on the mechanical activity of longitudinal and circular muscle strips isolated from the carp intestinal bulb (Cyprinus carpio). 198 39


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