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)

The present report concerns the immunocytochemistry of various peptide hormones and in particular their location in nervous structures. However, since the hormones observed in the neuroadenohypophysis and the digestive tractus have been examined elsewhere, they have been excluded from this study, except when considered outside there precise areas. The immunocytology of the following neuropeptides is presented, especially the particular details related to their demonstration: 1) The hypothalamic hypophysiotropic factor: LH-RF, SRIF, TSH-RF; derivatives from the so-called proopiocortine found by Mains and Eipper (1977), namely beta-LPH, enkephalins, endorphins, alpha-MSH- and ACTH-like antigens; 2) Prolactin and somathormone found outside the pituitary; 3) Gastro-intestinal hormones and their location outside the digestive hormones and their location outside the digestive mucosa, namely VIP, CCK, substance P; 4) Angiotensin II in nervous structures; 5) Neurotensin; 6) Thyrocalcitonin; 7) Relaxin, and the problem of its presence in the adult male genital tract. New data in invertebrate located vertebrate neuropeptides-like antigens in the nervous structures of pro-chordates (Ascidians) insects, crustaceans, annelids. These last findings underline the extensive significance of such hormonal molecules previously considered to be specific for vertebrates.
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PMID:Immunocytochemistry of polypeptide hormones: a review. 616 60

To test the hypothesis that enkephalins, substance P, bradykinin and angiotensin II could act as neurohumoral modulators of hypothalamic function, these peptides (0.01-20 microgram) were injected into the general circulation of anesthetized rats, and changes in hypothalamo-neurohypophysial activity were determined by continuously monitoring the amplitude of antidromic compound action potentials (CAP) in the hypothalamo-hypophysial tract. A decrease of CAP amplitude was taken to indicate an increase of orthodromic impulse traffic. All peptides elicited a CAP decrease. On a molar basis when injected i.v., the enkephalin analog FK 33-824 was the most effective substance, followed by substance P, Leu-enkephalin and angiotensin II. Enkephalins and substance P injected through the internal carotid artery, were 2-5 times more effective than when injected i.v., whereas bradykinin was most effective when it reached the brain through a vertebral route. Angiotensin II produced the same CAP decrease irrespective of the route of administration and, in contradistinction to the other peptides, its effect was not abolished by stalk section. Tachyphylaxis and reversibility with naloxone was observed only for the enkephalins. The data suggest that sites of action are the hypothalamus for enkephalins and substance P, the neurohypophysis for angiotensin II, and the hindbrain for bradykinin.
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PMID:Enkephalins, substance P, bradykinin and angiotensin II: differential sites of action on the hypothalamo-neurohypophysial system. 616 30

In the neonatal rat spinal cord slice preparation responses of the dorsal horn interneurons to iontophoretic or bath application of methionine-enkephalin (ME), substance P (SP) and somatostatin (SS) were qualitatively similar to those obtained in intact spinal cord. Thus, SP powerfully excited almost all neurons tested (15/16), while ME and SS depressed neuronal discharges in 13/14 and 4/6 units respectively. In some dorsal horn neurons the iontophoretic application of ME caused a marked depression of the SP-induced excitation. Angiotensin II (AgII) had no effect on dorsal horn units (n = 8). In the slices perfused with a Ca2+-free, Mg2+-high Krebs solution the extracellularly recorded effects of ME, SP and SS were not significantly modified, suggesting that the peptides were acting directly on postsynaptic sites. The results also indicate that the in vitro rat spinal cord slice preparation can be successfully utilized for further studies on the cellular mechanisms of actions of neuropeptides, particularly in relation to synaptic transmission processes in the dorsal horn.
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PMID:Neonatal rat spinal cord slice preparation: postsynaptic effects of neuropeptides on dorsal horn neurons. 616 14

There are now about twelve substances, many of them peptides, that are thought to act as neurotransmitters in the enteric nervous system. Most of the studies of peptides have relied on immunochemical methods for their detection. However, difficulties arise in these studies because of the close similarities between peptides. Related peptides can be grouped in several ways according to similarities of origin, function, effects in bioassays and amino acid sequences. Peptides with the same function in different species, and only slight differences in amino acid sequence, have been called isopeptides. Peptide families that have sequences of amino acids in common, but do not necessarily have similar functions are described. In the guinea-pig small intestine, used as a model, the concentrations of fourteen nerve-related peptides and amines are compared. The actual chemical natures of the peptides are discussed. It is concluded that nerves containing authentic leu- and met-enkephelin, somatostatin and substance P are present. VIP in guinea-pig enteric nerves is different from the porcine standard. Peptides similar to authentic CCK8 and amphibian skin bombesin are present. Angiotensin and neurotensin-like peptides shown immunohistochemically are not the authentic peptides. In the longitudinal muscle plus myenteric plexus, most neuropeptide concentrations are in the range of 10-500 pmole/g. The exception is met-enkephalin (1,300 pmole/g). The amine transmitters have considerably higher concentrations, noradrenaline having a concentration of about 3,500 pmole/g and acetylcholine 1-2 x 10(5) pmole/g.
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PMID:Detection and characterisation of neurotransmitters, particularly peptides, in the gastrointestinal tract. 617 12

A number of neuropeptides have been found to affect fluid intake when injected directly into the brain of various vertebrate species. These include: angiotensin II and its peptide precursors; the tachykinins Substance P, eledoisin and physalaemin; the opioid peptides met- and leu-enkephalin and beta-endorphin; bombesin; neurotensin; and vasopressin. Some of these stimulate drinking, some inhibit water intake, and the tachykinins have opposite effects on thirst depending on the species tested. Very little is known about the site or mechamism of action of most of these peptides or if their effects on thirst are physiological. The exception is angiotensin II, a peptide hormone that is synthesized in the blood in response to hypovalaemia or hypotension and is involved in many aspects of the regulation of blood volume and pressure. Angiotensin II injected intravenously or intracranially stimulates drinking in all reptiles, birds and mammals tested. In addition to its role as a hormone, angiotensin II may also function as a neurotransmitter or neuromodulator, since all of the enzymes and precursors necessary for its synthesis have been found in the central nervous system.
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PMID:Neuropeptides and thirst. 658 33

Intracellular recordings were made from isolated left or right stellate ganglia of Wistar rats and the morphology of neurones studied after intracellular injection of hexammine cobaltic chloride or back-filling from the post-ganglionic nerve with cobalt lysine complex. The experiments attempted to identify the location, electrophysiological properties, morphology and chemosensitivity of putative cardiac neurones in the ganglion. These were identified by antidromic activation of the axon in a cardiac nerve and compared with neurones projecting towards the brachial plexus (non-cardiac neurones). Putative cardiac neurones were localized in the ganglion around the postganglionic nerve entry zone and showed considerable morphological diversity. They had complex dendritic trees with, on average, seven dendrites. They included both phasic and tonic neurones and were depolarized by muscarinic agonists, angiotensin and substance P; they invariably had a synaptic input from the sympathetic trunk and from a T1 or T2 ramus and, in 16% of cells, from a cardiac nerve. Non-cardiac neurones were more widely scattered through the stellate ganglion but were not clearly different in morphology, resting membrane potential or the proportion of phasic and tonic cells from putative cardiac neurones. They also showed depolarizing responses to muscarinic agonists, angiotensin and substance P. Angiotensin responses of stellate ganglion cells were blocked by the peptide antagonist, saralasin (1 microM).
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PMID:Properties of putative cardiac and non-cardiac neurones in the rat stellate ganglion. 751 22

[3H]Senktide, a highly selective tachykinin NK3 receptor agonist, was used to study tachykinin NK3 receptors of rat and guinea pig brain. Guinea pig brain membranes had a Kd of 3.9 +/- 0.5 nM and a Bmax of 42 fmol/mg. Dose-displacement experiments with neurokinins and selective tachykinin receptor agonists revealed the following order of potency: [MePhe7]neurokinin B > neurokinin B > substance P > neurokinin A. This order is typical for a tachykinin NK3 receptor. To further characterize the specificity of this receptor, the effects of unrelated compounds such as: bradykinin, angiotensin II, bombesin and their structural analogs were also evaluated on the binding of [3H]senktide. Unexpectedly, the angiotensin AT1 receptor antagonists, DuP 753 (2-n-butyl-4-chloro-5-hydroxymethyl-1-[2'-(1H-tetrazol-5-yl)bip hen yl-4-yl)methyl]imidazole potassium salt), L-158,809 (5,7-dimethyl-2-ethyl-3-[(2'-(1H-tetrazol-5-yl) [1,1'-biphenyl]-4-yl) methyl]-3H-imidazo[4,5-beta]pyridine H2O) and EXP 3174 (2-n-butyl-4-chloro-1-[2'-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl]i midazole- 5-carboxylic acid), inhibited the binding of [3H]senktide to its receptor in the guinea pig brain membranes with IC50 values of 18 microM, 25 microM and 50 microM, respectively. Similar effects were also observed with rat brain membranes. Angiotensin II, saralasin ([Sar1,Val5,Ala8]angiotensin II, a peptide angiotensin AT1 receptor antagonist) and PD 123,319 (1-[4-(dimethylamino)3-methylphenyl]methyl-5-(diphenylacetyl)-4,5, 6,7- tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid, a known non-peptide angiotensin AT2 receptor antagonist) did not inhibit the binding of [3H]senktide to either type of membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-peptide angiotensin receptor antagonists bind to tachykinin NK3 receptors of rat and guinea pig brain. 751 91

1. The effect of topical betamethasone upon skin blood flow was investigated in the rat. Two types of vasodilator stimuli were used; local heating to the surface of the skin and intradermal application of inflammatory agents. Blood flow was measured by laser doppler velocimetry. 2. Topical betamethasone-17-valerate (1 g with an 18 h pretreatment) significantly inhibited the heat-induced vasodilatation in the rat skin, as also did systemically administered betamethasone (1 mg kg-1, 3 h pretreatment). 3. Angiotensin converting enzyme (ACE) inhibitors (captopril, 5 mg kg-1 and enalapril, 1 mg kg-1, 30 min pretreatments) were the only drugs out of several different types of systemically administered inhibitors and antagonists that were tested which also inhibited the heat-induced vasodilatation. Aprotinin (100,000 KIU kg-1, 5 min pretreatment) a serine protease inhibitor, significantly potentiated the heat-induced response. 4. Bradykinin (50 nmol per site), des-Arg9-bradykinin (5 nmol per site), substance P (0.1 nmol per site) and capsaicin (1 mumol per site) induced an increase in skin blood flow. 5. Topical betamethasone treatment resulted in a significant inhibition of the vasodilator response to des-Arg9-bradykinin, whereas captopril treatment inhibited the responses to substance P, capsaicin, bradykinin and des-Arg9-bradykinin. 6. Intradermal application of captopril (10-100 micrograms) also caused a dose-dependent inhibition of the heat-induced vasodilatation. 7. These results suggest that topical betamethasone may be acting in a manner similar to that of the ACE inhibitors to produce an inhibition of the flow responses in the skin and that this effect may be brought about by interfering with the action of vasodilator peptide(s) or protein(s).
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PMID:Investigations into the mechanism of vasoconstrictor action of the topical steroid betamethasone-17-valerate in the rat. 844 1

Angiotensin converting enzyme (ACE) -inhibitors inhibit degradation of inflammatory mediators substance P (SP) and bradykinin, which may further stimulate the synthesis of prostaglandins. The resulting increase in inflammatory mediators in tissues is suggested to be the reason for the dry cough, involving sensory C-fiber activation, among patients receiving ACE-inhibitor therapy. In the present study, the effect of an ACE-inhibitor, captopril, on ocular irritative responses was studied in the rabbit. Intravenous captopril decreased markedly the blood pressure and the intraocular pressure (IOP) modestly. Topical neutral formaldehyde elicits an irritative response in the eye mediated through sensory neuropeptides SP and calcitonin gene-related peptide (CGRP). Following topical neutral formaldehyde, the increase in IOP and breakdown of the blood-aqueous barrier were inhibited by captopril, while miosis was not affected. Cyclic AMP (cAMP) content in the aqueous humour was increased by captopril, and this increase was inhibited by indomethacin. Following YAG-laser anterior capsulotomy, captopril inhibited the increase in IOP, breakdown of the blood-aqueous barrier and miosis. The present study demonstrates that use of short-term administration of captopril prior to sensory nerve stimulation or YAG laser anterior capsulotomy does not enhance the ocular responses to these stimuli in the rabbit. In the present study, captopril inhibited these responses, at least partly by decreasing the blood pressure.
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PMID:Effect of captopril on ocular irritative response to topical neutral formaldehyde and YAG-laser capsulotomy in the rabbit. 859 Feb 56

In addition to their well characterized effects at dopamine receptors, neuroleptic drugs have been shown to affect the level and in vitro metabolism of neuropeptides. In the present study, the effect of acute and subchronic administration of the neuroleptic haloperidol and the nonselective, dopamine agonist apomorphine on neuropeptidase activity was determined in regional, rat brain P2 membranes. Subchronic administration of haloperidol decreased the activity of aminopeptidase N in the frontal cortex and caudate-putamen. In contrast, subchronic administration of apomorphine increased aminopeptidase N activity in the frontal cortex and caudate-putamen. Neutral endopeptidase 24.11 also was affected differentially in the caudate-putamen, but both subchronic haloperidol and apomorphine decreased neutral endopeptidase 24.11 activity in the frontal cortex. Metalloendopeptidase 24.15 activity was decreased in the caudate-putamen after acute haloperidol and increased in the frontal cortex after acute apomorphine administration; however, no effect was noted after subchronic administration of either drug. Angiotensin converting enzyme was not affected by any treatment. Therefore, neuroleptic-induced alterations in aminopeptidase N, neutral endopeptidase 24.11 and metalloendopeptidase 24.15 activity may account for previously reported alterations in neuropeptide degradation. In view of the interaction between mesocorticolimbic dopamine neurons and neuropeptides, e.g., substance P, neurotensin and enkephalins, neuroleptic-induced alterations in the activities of neuropeptidases, and thus neuropeptide metabolism can, in turn, play a role in modulating midbrain dopaminergic activity.
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PMID:Haloperidol and apomorphine differentially affect neuropeptidase activity. 861 7


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