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)

Prostaglandin synthesis by astrocytes in culture has been shown to be stimulated by a range of mediators including ATP, interleukin-1 and the neuropeptide substance P. In this paper we present evidence that astrocytes from rat spinal cord, but not other CNS regions, release prostaglandins in response to treatment with sub-micromolar concentrations of the neuropeptide substance P, a neuromodulator that may be involved in regulating the input of nociceptive information into the spinal cord. This in vitro phenomenon, if representative of physiological responses, suggests that astrocytes may play a role in central processing of noxious input. The fact that astrocytes from rat cortex do not exhibit substance P-evoked prostanoid release provides further evidence for regional astrocyte heterogeneity.
Adv Prostaglandin Thromboxane Leukot Res 1991
PMID:Eicosanoid synthesis by spinal cord astrocytes is evoked by substance P; possible implications for nociception and pain. 170 83

An in vitro testis-superior spermatic nerve preparation was used to evaluate the effects of chemical agents applied in the bathing solution. Both directly evoked discharges and responses to algesic solutions [bradykinin (BK) 9 X 10(-8) M, hypertonic saline 616 mM and high K+ solution 60 mM] of polymodal receptors were studied. Prostaglandin (PG)-E2 (1.4 X 10(-6)-1.4 X 10(-5) M) and serotonin (5-HT) (1.1 X 10(-6) to 1.4 X 10(-4) M) had only a weak excitatory effect. However, test responses to algesic substances were regularly greatly increased by PG-E2, -I2 and 5-HT. Concentrations of PG-E2 of 1.4 X 10(-8) M or greater augmented BK responses; higher concentrations and/or longer applications were needed to enhance responses to algesic salt solutions. Effective concentrations for the PGs and 5-HT were near those reported for inflamed tissues and exudate. Aspirin (ASA) (5.5 X 10(-4) M or greater, for more than 4 min) suppressed the responses to BK but not those evoked by hypertonic saline. The ASA effect on the BK response was largely restored by an addition of PG-E2. Substance P also had a weak excitatory effect on some polymodal receptors, but no significant enhancement of the response to BK was noted. These results further support a role of polymodal receptors in transmitting nociceptive information, of inflammatory origin.
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PMID:Effects of prostaglandins and other putative chemical intermediaries on the activity of canine testicular polymodal receptors studied in vitro. 243 85

Stretching of the renal pelvic wall activates renal mechanosensitive neurons, resulting in an increase in afferent renal nerve activity (ARNA). Prostaglandin (PG)E(2) plays a crucial role in the activation of renal mechanosensitive neurons through facilitation of the release of substance P from the sensory neurons in the renal pelvic wall. Because wall stretch may induce cyclooxygenase-2 activity, we examined whether cyclooxygenase-2 was expressed in the renal pelvic wall and whether activation of cyclooxygenase-2 contributed to the ARNA response produced through increased renal pelvic pressure. In situ hybridization showed a strong cyclooxygenase-2 mRNA signal in the papilla and subepithelial layer of the renal pelvic wall from time control kidneys and from kidneys exposed to 15 minutes of increased renal pelvic pressure in anesthetized surgically operated rats. In anesthetized rats, an increase in renal pelvic pressure increased ARNA by 40+/-2% and increased renal pelvic release of PGE(2) from 289+/-46 to 1379+/-182 pg/min (P<0.01). Renal pelvic perfusion with the cyclooxygenase-2 inhibitor etodolac reduced the increases in ARNA and PGE(2) by 66+/-7% and 55+/-13%, respectively (P<0.01). Likewise, the cyclooxygenase-2 inhibitor 5, 5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone reduced the increases in ARNA and PGE(2) by 43+/-5% and 47+/-8%, respectively. We conclude that cyclooxygenase-2 is expressed in the renal pelvic wall and that the activation of cyclooxygenase-2 contributes to the stimulation of renal mechanosensitive neurons in the pelvic wall.
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PMID:Cyclooxygenase-2 involved in stimulation of renal mechanosensitive neurons. 1064 27

Aseptic loosening remains the primary cause of failure in total joint arthroplasty. Implant-derived particles are thought to be a main cause of osteolysis that leads to failure of total joint arthroplasty. The nervous system has been implicated in the etiology and pathogenesis of joint diseases. Substance P (SP) immunoreactive nerve fibers have been detected in the pseudomembrane and pseudocapsular tissues of aseptic loose hip prostheses, suggesting that SP might be involved in the process of aseptic loosening. Fibroblasts are abundant in periprosthetic membrane. Neuropeptides are able to modulate cytokine production by fibroblasts. In this study, we isolated fibroblasts from periprosthetic membrane at the time of revision hip arthroplasty performed because of aseptic loosening. Fibroblasts were stimulated with titanium (Ti) particles or SP. Prostaglandin (PG) E2 and interleukin-6 (IL-6) assays were performed using enzyme-linked immunosorbent assay kit. PGE2 and IL-6 secretion by fibroblasts have been significantly increased in the presence of Ti particles or SP. Moreover SP caused significant increase in PGE2 and IL-6 production by Ti particles-stimulated fibroblasts. Thus, SP and Ti particles acted synergistically to increase PGE2 and IL-6 secretion in fibroblasts from periprosthetic membrane.
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PMID:Substance P augments PGE2 and IL-6 production in titanium particles-stimulated fibroblasts from hip periprosthetic membrane. 1745 May 84