Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal sensory responses and reflex function were examined in rats 24 h after 45 min of ischemic injury caused by unilateral renal arterial occlusion (RAO). The integrity of renal pelvic mechanoreceptor (MRu)-mediated renorenal reflex was examined. An increase in ipsilateral afferent renal nerve activity (ARNA) and a reflex decrease in efferent renal nerve activity (ERNA) and contralateral diuresis and natriuresis produced by increasing the intrapelvic pressure were seen in sham-operated (Sham) rats, but it was largely attenuated in RAO rats. Using single-fiber recordings of the renal MRu discharge, graded increases in intrapelvic pressure or renal pelvic administration of substance P (SP) resulted in pressure- or concentration-dependent increases in ARNA in the control kidney of Sham rats, whereas attenuated responses were seen in the postischemic kidney of RAO rats. The unresponsiveness of renal MRus in RAO rats was accompanied by an insufficient release of SP. However, the baseline SP release is higher in RAO kidneys due to a reduced neutral endopeptidase (NEP) activity in the renal pelvis of the postischemic kidney. No changes in NK-1 receptor mRNA levels were demonstrated; however, the expression of NK-1 receptors in the plasma membrane of RAO pelvis were decreased, possibly resulting from the internalization of the receptors associated with beta-arrestin trafficking. Renal excretory responses after saline loading were significantly lower in the postischemic kidney of RAO rats than in Sham rats. Responses of ARNA and ERNA were also lower. It is concluded that the defective activation of renal sensory mechanoreceptors in the postischemic kidney results from an inadequate release of SP after mechanostimulation and the reduced functional NK-1 receptors.
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PMID:Impaired renal sensory responses after renal ischemia in the rat. 1208 83

The effects of quercetin on substance P-induced plasma protein extravasation (PE) in the rat dura mater, cerebellum, olfactory bulb and cortex and also its modulation by endopeptidases, angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP) were studied. PE was assessed by photometric measurement of extravasated Evans blue. Substance P (SP) and NEP or ACE inhibitors increased the PE in dura mater. Pretreatment with captopril or phosphoramidon potentiated PE induced by SP in the dura mater and cerebellum, respectively. Quercetin increased the PE in the dura mater, cerebellum and cortex. Further results suggested that the PE induced by SP in the dura mater was enhanced by pretreatment with quercetin, similar to that observed with selective peptidase inhibitors. Quercetin-stimulated extravasation in all tissues was abolished by NK-1 receptor blockade. These results suggest that quercetin increases PE in the dura mater and CNS tissues by inhibiting NEP and/or ACE, showing that the effect induced in the dura mater, cerebellum and cortex occurs through endogenous SP accumulation.
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PMID:Effect of quercetin on plasma extravasation in rat CNS and dura mater by ACE and NEP inhibition. 1223 12

Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and beta2-microglobulin immunoreactivity were up-regulated and detected ectopically, indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.
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PMID:Probing the effects of stress mediators on the human hair follicle: substance P holds central position. 1805 48

Substance P has a stimulating effect on fibroblast proliferation, collagen organization, and angiogenesis in ruptured and subsequently sutured rat Achilles tendon. This effect is also reflected in the biomechanical properties of the tendon. The aim of this study was to substantiate the effect of exogenous substance P on endogenous substance P, NK-1 receptor, and nerve ingrowth in an in vivo tendon-healing setting. Ninety-six male Sprague-Dawley rats were randomly assigned to one of four groups and injected with saline, substance P (10(-6) micromol/kg BW and 10(-8) micromol/kg BW) associated with neutral endopeptidase inhibitors, or neutral endopeptidase inhibitors alone into the paratendinous region of the ruptured and subsequently sutured Achilles tendons from the second until the sixth day postoperatively. Substance P, NK-1 receptor, and nerve ingrowth (PGP 9.5) were analysed using immunofluorescence at four different time points: one, two, four and six weeks postoperatively. In all groups substance P was predominantly expressed in the extracellular matrix during the first two weeks, corresponding to fibroblast proliferation, and first disappeared from the saline group in the proliferative phase. In contrast, substance P was not expressed in the blood vessel wall during the first two weeks, when angiogenesis was most pronounced. NK-1 receptor was almost always expressed in the blood vessel wall and in the extracellular matrix during this period and disappeared progressively afterwards. No nerve ingrowth was identified. Exogenously administered substance P in sutured rat Achilles tendon rupture does not stimulate sensory nerve ingrowth, but seems to have a booster effect on endogenous substance P for fibroblast proliferation via autocrine/paracrine stimulation.
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PMID:Qualitative analysis of substance P, NK1-receptor and nerve ingrowth in substance P-treated ruptured rat Achilles tendon. 2069 62


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