Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that a number of peptides may be involved in the transmission of pain. In order to evaluate the possible role of peptides in the development of headache, we have, in the present study, examined the presence of nerve fibres containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) in human temporal and occipital tissues. In the skin, delicate VIP, SP and CGRP fibres occur beneath the epidermis, sometimes running into the folds of the dermal ridges. In deeper layers of the dermis, small blood vessels are occasionally surrounded by single nerve fibres containing NPY, VIP, SP and CGRP. Large temporal and occipital arteries are surrounded by a meshwork of such fibres. In addition, NPY and VIP fibres are seen around sweat glands and hair follicles. Smooth muscle bundles in the dermis are surrounded by VIP fibres, whereas the temporal muscle per se is devoid of such fibres.
Pain 1986 Dec
PMID:Peptide-containing nerve fibres in human extracranial tissue: a morphological basis for neuropeptide involvement in extracranial pain? 243 70

A unique pain syndrome, triggered by gustatory stimuli in the absence of anatomic obstruction of the parotid duct, complicated carotid endarterectomy. We documented asymmetric parotid vasodilatation and sympathetic dysfunction in cutaneous areas overlaying the gland. We postulate that damage to the sympathetic innervation of the parotid gland resulted in unopposed parasympathetically mediated glandular vasodilatation. Vasoactive intestinal polypeptide may have played a role in producing symptoms. A similar syndrome occurs in patients with acute pandysautonomia.
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PMID:Gustatory pain: a complication of carotid endarterectomy. 254 53

Octreotide is a long-acting cyclic octapeptide with pharmacologic actions mimicking those of the natural hormone somatostatin. It can suppress the secretion of serotonin, as well as the gastroenteropancreatic peptides gastrin, vasoactive intestinal peptide (VIP), insulin, glucagon, secretin, motilin, and pancreatic polypeptide. It also suppresses growth hormone and decreases splanchnic blood flow. Octreotide is completely and rapidly absorbed following subcutaneous injection and has an elimination half-life of 1.5 hours. Clinical trials reviewed here show octreotide useful in the treatment of diarrhea associated with VIP secreting tumors, as well as diarrhea and flushing associated with carcinoid syndrome, both conditions for which the drug is approved. Clinical trials involving the use of octreotide in the treatment of acromegaly are also reviewed. Adverse reactions to octreotide are mild to moderate and most commonly involve injection site pain and diarrhea. Drug interactions are apparently related to the drug's pharmacologic effects. Octreotide is given subcutaneously two to three times daily, with daily doses ranging from 50mcg to 1,500mcg per day. Further research appears necessary to clarify dosing issues.
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PMID:Debut of a somatostatin analog: octreotide in review. 255 39

The chemistry, pharmacology, pharmacokinetics, clinical uses, adverse effects and drug interactions, dosage, availability and cost, and indications for use of octreotide, a new synthetic analogue of the peptide hormone somatostatin (SS), are reviewed. Like SS, octreotide suppresses secretion of pituitary growth hormone (GH) and thyrotropin and decreases release of a variety of pancreatic islet cell hormones including insulin, glucagon, and vasoactive intestinal peptide (VIP). Octreotide also reduces splanchnic blood flow, gastric acid secretion, GI motility, and pancreatic exocrine function and alters the absorption of water, electrolytes, and nutrients from the GI tract. The elimination half-life of i.v. octreotide is 72-98 minutes, compared with 2-3 minutes for i.v. SS. Usual administration of octreotide is by the i.v. or s.c. route. Octreotide has been studied in the treatment of hormone-secreting pituitary tumors and pancreatic islet cell tumors. Octreotide therapy lowers GH secretion and improves clinical symptoms in patients with acromegaly and may suppress clinical symptoms to a greater degree than bromocriptine. Patients with carcinoid syndrome and VIP-secreting tumors (vipomas) have had substantial improvement in clinical symptoms with administration of octreotide. This agent does not appear to be effective in the treatment of nonvariceal upper GI bleeding and acute pancreatitis; its relative usefulness in the treatment of variceal bleeding is not established. Adverse effects associated with octreotide therapy generally have been mild, including pain or burning at the injection site, abdominal pain, and diarrhea. Octreotide has been shown to interfere with absorption of oral cyclosporine. Standard initial therapy is octreotide acetate 50-100 micrograms s.c. every 8-12 hours, with titration based on clinical and biochemical effects. Up to 3000 micrograms/day of octreotide acetate has been administered to patients with acromegaly without serious adverse effect. Octreotide is marketed under the brand name Sandostatin and is available in 1-mL ampuls containing 50, 100, and 500 micrograms of octreotide acetate. Because the conditions for which octreotide appears to be most effective are uncommon, the drug should be considered for addition to the formulary in tertiary-care institutions only; addition of octreotide to the formulary of a community hospital is probably unnecessary. The synthetic analogue octreotide is longer acting and more specific in pharmacologic action than SS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Octreotide, a new somatostatin analogue. 265 11

Neural factors influence post-natal growth, development, and aging throughout the body. This influence may be mediated through sensory or motor effects interacting with endocrine and immunological factors. Growth effects may be expressed directly by sensory or motor nerves on the tissue or indirectly by motor function. Direct neutrotrophic effects have been well-documented in the development of striated muscle, the taste bud, and the amphibian limb. Evidence for a trigeminal neurotrophic effect on tooth development and facial development is lacking. Growth disturbances of the jaws consequent to lesioning of the trigeminal nerve are due most likely to functional disturbances rather than neutrotrophism. Examples of function impact on orofacial growth are abundant. Oral and facial target tissues, like those elsewhere in the body, determine the nature of the target tissue innervation and its central organization. Central effects consequent to tooth loss or dental pulp entirpation are well-documented. Inflammation and pain may exert growth effects through release of "wound hormones" or secondarily to somatic and autonomic effects. There is evidence that vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) elaborated from sympathetic and parasympathetic neurons may have a modulatory role in growth. While the effects of longstanding motor pathologies on skeletal growth are well-known, concomitant sensory deficits and soft tissue disturbances have not been examined. However, the pathological models beg the question of normal regulation. While muscle develops in the absence of innervation, neurotrophic effects are clearly identified. Little is known about the interaction of simple and complex motor behavior on growth. Regulation of growth is frequently visualized within a form-function paradigm. For example, anterior open bites have been seen as the consequence of tongue thrusting or tongue thrusting as a consequence of open bites. Low tonic forces in posture are thought to be more important in the development of both the face and the dental alveolar complex than the higher intermittent forces in mastication and swallowing. The need for an active (reflex) contribution to growth at the TMJ is in dispute.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Growth, development, and aging of orofacial tissues: neural aspects. 269 Aug 47

The distribution, ontogeny and fiber projections of cholecystokinin-8, vasoactive intestinal polypeptide and gamma-aminobutyrate-containing neuronal systems in the rat spinal cord were investigated by means of immunocytochemistry. Immunoreactive fibers to cholecystokinin-8, vasoactive intestinal polypeptide and glutamate decarboxylase (gamma-aminobutyrate-synthesizing enzyme, used as a marker of gamma-aminobutyrate) were widely distributed in the spinal cord, being particularly concentrated in the superficial dorsal horn, suggesting a close relationship to the pain transmission system. Cholecystokinin-8-containing neurons were mostly distributed in the dorsal laminae and glutamate decarboxylase-containing neurons were distributed in both the dorsal and ventral horns. Vasoactive intestinal polypeptide-containing neurons were detected in the lateral spinal nucleus and the lamina X. Cholecystokinin-8 and vasoactive intestinal polypeptide immunoreactive structures first appeared on gestational day 17-18. Although no substantial change in immunoreactive structures was observed during the fetal period, they increased markedly after birth. On the other hand, glutamate decarboxylase-positive structures appeared at gestational day 16 and those in the grey matter reached a maximum content at birth; both groups were present in adult animals. Transection of the upper cervical cord resulted in accumulations of cholecystokinin-8 and glutamate decarboxylase rostral to the lesion, revealing the presence of supraspinal projections of cholecystokinin-8 and glutamate decarboxylase to the spinal cord. The same experimental procedure demonstrated the existence of vasoactive intestinal polypeptide-mediating neuronal projections to the supraspinal level, as the accumulating fibers occurred in the area caudal to the lesion.
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PMID:Distribution, ontogeny and projections of cholecystokinin-8, vasoactive intestinal polypeptide and gamma-aminobutyrate-containing neuron systems in the rat spinal cord: an immunohistochemical analysis. 388 8

The effects of a number of vasoactive and neurotransmitter substances on lymphocyte traffic were studied by assessing their effects on the release of lymphocytes into primary peripheral (popliteal) nodal efferent lymph of sheep following acute infusion into cannulated afferent nodal lymphatics. In a total of 23 experiments, the output of lymphocytes, small and blast, was increased by serotonin, substance P, bombesin, [met]enkephalin, isoprenaline and phenylephrine and was decreased by vasoactive intestinal peptide (VIP), neurotensin and carbachol. Substances whose actions are modulated by prostaglandins and enhanced by prostaglandin synthesis inhibitors and which elevate blood monocyte and nervous tissue levels of cyclic GMP tended to increase lymphocyte traffic through peripheral lymph nodes in sheep in vivo. The opposite effect tended to be produced by substances whose actions require or are associated with prostaglandins or histamine, and which affect blood monocytic cyclic nucleotide levels by elevation of cyclic AMP or depression of cyclic GMP. Pain and inflammation tended to increase lymphocyte traffic, while analgesics and immunomodulators tended to decrease it.
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PMID:Modification of lymphocyte traffic by vasoactive neurotransmitter substances. 614 65

Intrathecal injections of capsaicin (CAP) and 4 other homovanillic acid (HMV) derivatives related to the structure of CAP were carried out. Capsaicin, 1-nonenoylvanillylamide (NVA), HMV-dodecylamide (DCA) (but not HMV-cyclohexylamide (CHA) or HMV-hexadecylamide (HDC] reduced the spinal content of substance P (SP), as measured by radioimmunoassay (RIA), and increased the tail-flick latency. Similar injection of kainic acid and piperine reduced levels of SP but failed to affect the tail-flick latency. None of the agents used affected spinal levels of cholecystokinin (CCK) or vasoactive intestinal peptide (VIP) as measured by RIA. In experiments using in vivo superfusion of the rat spinal cord, CAP, DCA and NVA were found to stimulate release of SP. Capsaicin had no effect on the levels of CCK or VIP immunoreactivity in the spinal superfusate. A tachyphylaxis to the effect of CAP and DCA on spinal SP release was demonstrated. Pretreatment with either agent blocked the releasing effect of the second. Pretreatment with an inactive analogue (HDC) had no effect on the subsequent activity of CAP. Kainic acid and piperine did not induce release of SP from the spinal cord. The relative selectivity of spinally administered capsaicinoids with regard to their effects on the content and release of peptides known to be contained in primary afferents and the presence of a similar structure-activity relationship for depletion and release of SP, desensitization and antinociception suggest the presence of a specific receptor site associated with a specific population of primary afferents through which pain information may pass. Whether SP is an 'afferent pain transmitter' is not clear, but at the least, it appears to serve as a marker for a population of afferents acted upon by spinally administered capsaicinoids.
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PMID:Action of intrathecal capsaicin and its structural analogues on the content and release of spinal substance P: selectivity of action and relationship to analgesia. 620 19

With the development of specific antibodies to vasoactive peptides and application of immunohistochemistry and radioimmunoassay methods, knowledge of vascular innervation has grown rapidly. In the cerebral circulation, four possible neurotransmitters are present: norepinephrine, acetylcholine, vasoactive intestinal peptide (VIP), and substance P. There is a dense adrenergic innervation of cerebral arteries, but contractile responses to nerve stimulation or circulating catecholamines are relatively small both in vitro and in vivo. Recent studies using radioligand binding techniques indicate a lack of specific 3H-prazosin binding in cerebral arteries, in contrast to other vascular beds. Thus a lack of alpha1-adrenergic receptors in cerebral arteries may account for weak responsiveness to sympathetic stimulation. Both VIP and acetylcholine may be vasodilator neurotransmitters, but blockade of cholinergic responses does not alter neurogenic vasodilation. The lack of specific VIP antagonists hampers efforts to explore this system more fully. Substance P-containing nerves are affected by capsaicin, supporting the hypothesis that these are primary sensory afferents, perhaps mediating pain. Future work in this area may focus on defining the pathways of these nerves and exploring the role of co-transmitters and possible interactions between nerves. With this basic information, experiments can be designed to elucidate more clearly the functional roles these nerves play.
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PMID:Innervation of the cerebral vasculature. 621 1

After immunohistochemical staining appendices without active inflammation but producing symptoms of appendicitis (N = 24) were compared with a control group of appendices removed incidental to another procedure (N = 26). Staining for neurone specific enolase (NSE) showed more instances of nerve 'hyperplasia' in the control group than in the appendices generating pain refuting the concept of neuroappendicopathy based on quantitative nerve changes. Serotonin staining identified subepithelial neuroendocrine cells (SNC) in 85 per cent of the specimens. All cases showed serotonin immunoreactive enterochromaffin cells (EC). Staining for serotonin was significantly decreased in the SNC in the painful group. There were no significant differences between the two groups in staining intensity of SNC and EC for substance P (SP). Vasoactive intestinal polypeptide (VIP) was not seen in the SNC and EC and there were no differences in nerve fibre staining for VIP. Serotonin is a neurotransmitter as well as mediator of inflammation. It is suggested that reduced staining for serotonin in painful appendices reflects discharge of stores which could be instrumental in inducing the pain in these cases. Continued serotonin release may then lead to acute appendicitis.
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PMID:Serotonin and its possible role in the painful non-inflamed appendix. 637


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