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)

Rat brain particulate fraction was found to contain binding sites for 125I-Salmon Calcitonin-I (125I-SCT). Maximum binding occurred in the physiological pH range of 7.25-7.5. The binding reaction proceeded in a temperature-dependent manner. Binding sites were broadly distributed among the various rat brain regions and considerable regional differences existed in the affinity and density as detected by Scatchard analysis. The highest affinity was recorded in the case of the hypothalamus and the lowest in the case of the cerebellum. The KD (nM) and Bmax (pmole/mg protein) estimated for the binding to four regions were as follows: hypothalamus: 1.4 and 0.19, midbrain, hippocampus plus striatum: 1.5 and 0.08, pons plus medulla oblongata: 3.0 and 0.15 and cerebellum: 8.3 and 0.20. Using a particulate fraction of rat brain void of cerebellum and cortices, a binding assay for calcitonins was developed. Binding of 125I-SCT was inhibited by unlabeled salmon, [Asu1,7]-eel and porcine calcitonins in a dose-dependent manner and the IC50s were 2.0, 8.0 and 30 nM, respectively. The IC50s were comparable to those estimated using a kidney particulate fraction. Human calcitonin, beta-endorphin and substance P were weak inhibitors of the binding. Other peptides, drugs and putative neurotransmitters tested (totally 23 substances) failed to inhibit the binding at concentrations of 1.0 microM. The physiological significance of brain binding sites for calcitonin, with the possibility that the brain may possess endogenous ligands for these sites are discussed.
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PMID:Specific binding of 125I-salmon calcitonin to rat brain: regional variation and calcitonin specificity. 725 44

Ultrastructural, immunocytochemical, and immunoelectron microscopical examinations are reported that describe the morphology of putative sensory nerve endings in the dura mater encephali of the rat and the cat. Morphometrical measurements and reconstructions showed that in the cat the mean diameter of axons, the bare area of axolemma, and the content of mitochondria and vesicles are highly variable in dural nerve endings. Nerve fibers with a high volume density of mitochondria are thought to be sensory, while nerve fibers containing many small vesicles are considered autonomic. There is, however, a broad overlap of mitochondria-rich and vesicle-rich nerve fibers in the dura, so that discrimination between sensory and autonomic endings by these characteristics frequently fails. Whole-mount preparations treated cytochemically for detection of substance P- and calcitonin gene-related peptide-like immunoreactivity in the rat and the cat showed a network of immunopositive nerve fibers in the vicinity of dural blood vessels. Most of these peptidergic and probably sensory nerve fibers were found terminating in the dural connective tissue far from vessels. Calcitonin gene-related peptide-positive nerve fibers were much more abundant than substance P-positive fibers. Immunoelectron microscopic preparations revealed that calcitonin gene-related peptide- and substance P-like immunoreactivity is found in a small proportion of generally thin unmyelinated nerve fibers. These proportions were very similar in the rat and the cat. Summarizing the recent literature, the morphological characteristics of putative sensory nerve fibers in the dura mater are discussed in relation to their possible functional significance for neurogenic inflammation and nociception.
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PMID:Innervation of the dura mater encephali of cat and rat: ultrastructure and calcitonin gene-related peptide-like and substance P-like immunoreactivity. 750 17

The prenatal and postnatal development of the innervation of the rat kidney has been investigated using immunocytochemical methods. The efferent innervation was studied using dopamine-beta-hydroxylase and neuropeptide Y antibodies. Calcitonin gene related peptide and substance P antibodies were used to investigate the afferent innervation. Kidneys from embryos of 14 to 20 days, from newborn rats, and from animals of 4, 10, 12, 21, 38, 60, and 90 days of age were studied. Slices of whole kidneys were analyzed, and frozen sections were used to investigate the location of the nerves in more detail. Both afferent and efferent nerves are observed inside the kidney by embryonic day 16. At birth, the afferent nerves are found (1) forming a rich plexus in the renal pelvis; (2) associated with the renal vasculature as far as the interlobular arteries (cortical radial arteries) and (3) in the corticomedullary connective tissue. The efferent innervation appears, at birth, to extend to the interlobular arteries and to the afferent arterioles of the perihilar juxtamedullary nephrons. The efferent innervation increases rapidly during the following days, and by postnatal day 21 a distribution of the innervation similar to that of the adult is observed. While the afferent innervation reaches the major target regions of the kidney by birth, the efferent does most of its expansion into the kidney postnatally. Afferent and efferent fibers are found, extrarenally and intrarenally, in the same nerve bundles. This proximity between afferent and efferent fibers may represent anatomical bases for their interaction in the adult as well as during development.
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PMID:The rat renal nerves during development. 750 1

Adenylate cyclase was stimulated by prostaglandin E2 (PGE2) and parathyroid hormone-related protein (PTHrP) in both these types of fibroblast and by calcitonin gene-related protein (CGRP) in the human fibroblasts in vitro. PGE2 (1 microM), CGRP (1 microM), and PTHrP (1 microM) stimulated adenylate cyclase up to 50-fold, 10-fold and 9-fold, respectively. Calcitonin (CT), substance P (SP), interleukin-1 beta (IL-1 beta), and transforming growth factor-beta 1 (TGF beta 1) had no effect on adenylate cyclase in either fibroblast. Intracellular Ca2+ (iCa2+) was measured in individual fibroblasts from the periodontal ligament using Indo-1 and an adherent cell analysis and sorting interactive laser cytometer. Ionomycin (3 microM) caused a transient rise of iCa2+ in all human and canine fibroblasts tested. The mean percentage increase in iCa2+ in response to ionomycin was 820 and 840% for human and canine fibroblasts, respectively. The human fibroblasts responded to PGE2 (1 microM) by an increased iCa2+ concentration; the mean percentage increase in iCa2+ was 187%. SP caused a less pronounced increase in iCa2+ in the human fibroblasts (56%). CGRP and SP caused a similar response in the canine fibroblasts. The mean percentage increase in iCa2+ in response to SP and CGRP was 95 and 78%, respectively. PTH, PTHrP, platelet-activating factor, CT, and IL-1 beta had no effect on iCa2+ in either type of fibroblast. The data indicate that cAMP and calcium have roles as intracellular secondary messengers in the action of PGE2, SP, CGRP, and PTHrP in fibroblasts of human and canine periodontal ligament.
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PMID:Effects of hormones and cytokines on stimulation of adenylate cyclase and intracellular calcium concentration in human and canine periodontal-ligament fibroblasts. 750 23

Calcitonin gene-related peptide (CGRP) and substance P (SP) immunoreactivity was examined in neurons of the monkey trigeminal ganglion. Moreover, CGRP- and SP-positive varicose nerve fibers were found, occasionally forming pericellular arborizations around trigeminal somata, which, at light microscopic level, suggested the existence of synaptic contacts. Electron microscopic investigation however, revealed that although these varicose fibers ran in close range of somata and were containing accumulations of CGRP- and SP-positive vesicles, classical synaptic contacts were not present.
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PMID:Calcitonin gene-related peptide and substance P immunoreactivity in the monkey trigeminal ganglion, an electron microscopic study. 750 50

Endoneurial hypoxia of ischaemic origin is believed to cause the reduction in sciatic nerve substance P levels in experimentally diabetic rats. The first part of this study was designed to determine whether the changes seen extended to another neuropeptide, calcitonin gene-related peptide, and to reveal any correlation between substance P and calcitonin gene-related peptide levels in the sciatic nerve of both diabetic and centrally hypoxaemic rats. Comparison of streptozotocin diabetic rats (four-week duration) with their control group showed clear reductions in both substance P-like immunoreactivity (control = 225 +/- 20 pg/mg protein, diabetic = 139 +/- 19; P < 0.01) and calcitonin gene-related peptide-like immunoreactivity (control = 9.08 +/- 0.65 ng/mg protein, diabetic = 4.43 +/- 0.44; P < 0.001). A similar pattern was seen with the comparison of five-week centrally hypoxaemic rats (housed in 10% O2) with their controls for both substance P-like immunoreactivity (control = 222 +/- 10 pg/mg protein, hypoxic = 148 +/- 13; P < 0.001) and calcitonin gene-related peptide-like immunoreactivity (control = 6.58 +/- 0.42 ng/mg protein, hypoxic = 3.01 +/- 0.45; P < 0.001). Calcitonin gene-related peptide levels correlated closely with substance P levels in both the diabetes and central hypoxaemia studies (r2 = 0.69 and 0.62, respectively). The second part of this study measured the messenger RNA levels of the substance P precursor, preprotachykinin-A, and calcitonin gene-related peptide messenger RNA in the L4 and L5 dorsal root ganglia of control, diabetic and centrally hypoxaemic rats. There was no change in preprotachykinin-A or calcitonin gene-related peptide messenger RNA levels between any of the groups, suggesting that the sciatic nerve decreases in substance P and calcitonin gene-related peptide described above are post-transcriptional in origin.
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PMID:Reduced sciatic nerve substance P and calcitonin gene-related peptide in rats with short-term diabetes or central hypoxaemia co-exist with normal messenger RNA levels in the lumbar dorsal root ganglia. 751 37

Trigeminal sensory nerves release neurotransmitters such as calcitonin gene-related peptide (CGRP), substance P, and others in human nasal mucosa. The effects of CGRP on nasal secretion were tested in humans in vivo by applying CGRP directly to nasal mucosa and then lavaging the nostrils ten minutes later. Concentrations of total protein, albumin, lysozyme, and orcinol-reactive mucoglycoconjugates were measured in lavage fluid. Calcitonin gene-related peptide (0.1 to 100 micrograms) did not stimulate secretion of any of these markers indicating that CGRP had no effect on glandular secretion or albumin exudation in vivo. These findings indicate that CGRP did not stimulate glands or endothelial cells of the vessels that regulate plasma extravasation. These data are consistent with previous studies that demonstrate 125I-CGRP binding sites on arterial vessels without detecting sites on glands or epithelium, the absence of effects of CGRP on glandular secretion from human nasal mucosal explants in vitro, and the apparently minor magnitude of sensory nerve axon responses in humans in vivo.
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PMID:Calcitonin gene-related peptide nasal provocation in humans. 751 5

Capsaicin at low concentrations increases the short circuit current (SCC) across frog skin. Simultaneous measurements of both transepithelial fluxes of 22Na or 36Cl demonstrate that the SCC increase is due to stimulation of sodium active absorption. Capsaicin acts through the liberation of several peptides; thus these peptides were tested on the SCC across frog skin. Those more active are, in order of potency: Cyclic Calcitonin Gene Related Peptide (CGRP), Kassinin and Eledoisin, Substance P (SP) and Neurokinin A. Neurokinin B and Vasoactive Intestinal Peptide (VIP) have no effect. Also the actions of SP and CGRP are due mainly to stimulation of Na+ active absorption. A strict parallelism regarding the sensitivity to inhibitors (Naproxen, SQ22536 and CP96345) between SP, CGRP and Capsaicin strengthens the hypothesis that SP and CGRP are liberated by Capsaicin in this tissue.
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PMID:Action of capsaicin and related peptides on the ionic transport across the skin of Rana esculenta. 751 33

Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. In this study patients with episodic cluster headache fulfilling the criteria of the International Headache Society were examined during an acute spontaneous attack of headache to determine the local cranial release of neuropeptides. Blood was sampled from the external jugular vein ipsilateral to the pain before and after treatment of the attack. Samples were assayed for calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), substance P and neuropeptide Y. Attacks were treated with either oxygen inhalation, sumatriptan or an opiate. Thirteen patients were studied of whom 10 were male and three female. All had well-established typical attacks of cluster headache when blood was sampled. During the attacks external jugular vein blood levels of CGRP and VIP were raised while there was no change in neuropeptide Y or substance P. Calcitonin gene-related peptide levels rose to 110 +/- 7 pmol/l (normal: < 40) while VIP levels rose to 20 +/- 3 pmol/l (normal: < 7). Treatment with both oxygen and subcutaneous sumatriptan reduced the CGRP level to normal, while opiate administration did not alter the peptide levels. These data demonstrate for the first time in vivo human evidence for activation of the trigeminovascular system and the cranial parasympathetic nervous system in an acute attack of cluster headache. Furthermore, it is shown that both oxygen and sumatriptan abort the attacks and terminate activity in the trigeminovascular system.
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PMID:Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies. 751 21

Achalasia is a disease of the esophagus characterized by incomplete relaxation of the lower esophageal sphincter, resulting in obstruction. Aperistalsis and dilation of the esophageal body occurs later, contributing to the esophageal dysfunction. Gastrointestinal bleeding in achalasia is an infrequent complication usually caused by stasis ulcer, esophageal varices, carcinoma, or pneumatic dilation of the sphincter. We describe here a patient with longstanding achalasia who bled vigorously from a proximal esophageal site that can be identified as arterial bleeding by endoscopy. Subsequent esophageal resection allowed detailed histological and immunohistochemical examination, which revealed a vascular ectasia. This lesion was associated with an unusually rich network of nerve fibers containing calcitonin gene-related peptide. Neuropeptide Y- and substance P-containing fibers were found to be decreased in this lesion as compared with controls. On the other hand vasoactive intestinal peptide- and nitric oxide synthase-containing fibers appeared quantitatively similar to those of controls. Calcitonin gene-related peptide is known to be involved in angiogenesis and may have played a causative role in the development of this lesion. Vascular ectasia may represent a hitherto unreported complication of achalasia.
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PMID:Innervation of an esophageal ectatic submucosal blood vessel in achalasia and a comparison with normals. 752 10


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