Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concept of neuro-immuno-cutaneous system (NICS) means narrow interrelations between nervous system, immunity and skin. Indeed, there are numerous cellular contacts between nerve fibers, cutaneous cells and immune cells; cutaneous cells can synthesize neuromediators and they express receptors to these molecules; neuromediators are able to modulate functions of cutaneous and/or immune cells. Using confocal or electron microscopy, connexions between nerve fibers and cutaneous cells have been observed. In the skin, nerve fibers may secrete neuromediators: substance P, vaso-active intestinal peptide (VIP), somatostatin, calcitonin-gene related peptide (CGRP), gastrin-releasing peptide (GRP), neuropeptide Y, peptide histidine-isoleucine (PHI), neurotensin, neurokinins A et B, bradykinin, acetylcholine, catecholamines, endorphins and enkephalins. Neurohormones such as prolactin, melano-stimulating hormone (MSH) or adreno-corticotrophic hormone (ACTH) are also expressed in the skin. Neuromediators and neurohormones are also secreted by cutaneous cells and these cells express receptors. Functions of epidermal or dermal cells are modulated by these substances. Immune cells transiently present in the skin (macrophages, lymphocytes...) are modulated by neuromediators through receptors. In the course of skin diseases, especially inflammatory diseases, the NICS is destabilized. Psoriasis and atopic dermatitis are good examples. This phenomenon might be due to inflammation but is also responsible for induction and maintenance of the inflammation.
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PMID:[Neuro-immuno-cutaneous system (NICS)]. 915 66

To evaluate the effect of bradykinin (BK) on rat islet alpha, beta, and delta cells, the rat pancreas was perfused in situ with BK (1 mumol/L) for 30 minutes via a cannula placed in the celiac artery. Insulin, glucagon, and somatostatin concentrations in the effluent were measured to determine the effect of BK on the secretion of these hormones. The BK concentration of the rat pancreas was also measured. Basal secretion of insulin, glucagon, and somatostatin in medium containing 6 mmol/L glucose was maintained at 6.5 +/- 0.5 ng/mL 124 +/- 8 pg/mL, and 511 +/- 22 pg/mL (n = 12), respectively. BK (1 mumol/L) induced a transient peak that was 3.7-fold of the baseline concentration within 3 minutes, followed by a sustained level that was approximately 50% higher than baseline. BK also transiently increased glucagon secretion with a peak that was 1.7-fold of the baseline concentration within 3 minutes, without a sustained secretion phase. BK caused a reduction in somatostatin secretion within 3 minutes to a level of 60% to 70% of the baseline concentration. The BK concentration of the rat pancreas was 3.42 +/- 1.45 micrograms/g protein (n = 5), which was approximately 3 mumol/L. We concluded that BK stimulated insulin secretion, transiently increased glucagon secretion, and decreased somatostatin secretion during the 30-minute perfusion of the rat pancreas.
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PMID:The effect of bradykinin on secretion of insulin, glucagon, and somatostatin from the perfused rat pancreas. 932 91

A chymostatin-sensitive angiotensin II-generating enzyme was found in human gastroepiploic arteries. The enzyme was purified using heparin affinity and gel filtration columns. The molecular mass of the purified enzyme was 30 kDa, and the optimum pH was between 7.5 and 9.0. Enzyme activity was inhibited by soybean trypsin inhibitor, phenylmethylsulfonyl fluoride and chymostatin, but not by ethylenediaminetetraacetic acid, pepstatin and aprotinin. The enzyme rapidly converted angiotensin I to angiotensin II (K(m), 67 mumol/l; Vmax, 43 pmol/s, kcat, 65/s), but did not hydrolyse angiotensin II, substance P, bradykinin, vasoactive intestinal peptide, luteinizing hormone-releasing hormone, somatostatin and alpha-melanocyte-stimulating hormone. The N-terminal sequence was identical to the sequence for human skin/heart chymase. Thus, the chymostatin-sensitive angiotensin II-generating enzyme in human vascular tissues is identified as chymase.
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PMID:Characterization of chymase from human vascular tissues. 935 25

1. Primary afferent nerve fibers control cutaneous blood flow and vascular permeability by releasing vasoactive peptides. These vascular reactions and the additional recruitment of leukocytes are commonly embodied in the term neurogenic inflammation. 2. Calcitonin gene-related peptide (CGRP) acting via CGRP1 receptors is the principal transmitter of neurogenic dilatation of arterioles whereas substance P (SP) and neurokinin A (NKA) acting via NK1 receptors mediate the increase in venular permeability. 3. Neurogenic vasodilatation and plasma protein leakage play a role in inflammation because many inflammatory and immune mediators including interleukin-1 beta, nitric oxide, prostanoids, protons, bradykinin, histamine, and 5-hydroxytryptamine can stimulate peptidergic afferent nerve fibers or enhance their excitability. 4. Neurogenic inflammatory reactions can be suppressed by alpha 2-adrenoceptor agonists, histamine acting via H1 receptors, 5-hydroxytryptamine acting via 5-HT1B receptors, opioid peptides, and somatostatin through prejunctional inhibition of peptide release from vasoactive afferent nerve fibers. CGRP, SP, and NKA receptor antagonists are powerful pharmacological tools to inhibit neurogenic inflammation at the postjunctional level. 5. Imbalance between the facilitatory and inhibitory influences on afferent nerve activity has a bearing on chronic inflammatory disease. Impaired nerve function represents a deficit in skin homeostasis while neuronal overactivity is a factor in allergic and hyperreactive disorders of the skin.
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PMID:Neurogenic vasodilatation and plasma leakage in the skin. 945 75

The effect of somatostatin on the sensory activity of primary afferents was studied in normal and acutely inflamed rat knee joints. Fine afferent nerve fibers with conduction velocities of 0.9-18.0 m/s were recorded as single units. All nerve fibers tested responded to local mechanical stimulation, movements of the joint and i.a. injections of KCl (10(-4) mol, 0.1 ml) close to the joint. Somatostatin (10(-4) mol, 0.2 ml) caused no direct response of the units. In normal joints, somatostatin did not change the discharges evoked by non-noxious movements but decreased the responses to noxious movements significantly to about 63% of the responses before the application. In acutely inflamed joints, somatostatin reduced the discharges of non-noxious and of noxious movements to about 55% and 52%, respectively. Injections of somatostatin with lower concentrations (10(-6) mol, 10(-8) mol) i.a. close to inflamed joints revealed shorter and less pronounced reductions of the responses to noxious movements. In a proportion of afferents, substance P (10(-4) mol) and bradykinin (10(-4) mol) were able to increase these responses again. These data indicate that the mechanosensitivity of articular afferents in normal joints may also be regulated by several neuropeptides based on a balance of pro-inflammatory peptides such as substance P, and anti-inflammatory peptides such as somatostatin. In an inflamed joint, pro-inflammatory peptides seem to predominate resulting in a sensitization of the peripheral nerve fibers. In this case, an application of somatostatin or its analogues could be used clinically to compensate this effect.
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PMID:Inhibitory effect of somatostatin on the mechanosensitivity of articular afferents in normal and inflamed knee joints of the rat. 946 28

Connections between nerve fibres and cutaneous cells have been studied using confocal and electron microscopy. In the skin, nerve fibres may secrete neuromediators, i.e. substance P, vasoactive intestinal peptide, somatostatin, calcitonin-gene-related peptide, gastrin-releasing peptide, neuropeptide Y, peptide histidine-isoleucine, neurotensin, neurokinins A and B, bradykinin, acetylcholine, catecholamines, endorphins and enkephalins. Neurohormones such as prolactin, melanocyte-stimulating hormone and adrenocorticotrophic hormone are also expressed in the skin. Neuromediators and neurohormones may be secreted by cutaneous cells, which also express receptors. Functions of epidermal and dermal cells are modulated by these substances. Immune cells transiently present in the skin (e.g. macrophages and lymphocytes) are modulated by neuromediators through receptors. During the course of skin disorders, especially inflammatory reactions, the neuroimmunocutaneous system is destabilized. This is particularly true in psoriasis. This destabilization may be secondary, although evidence shows it can also be responsible for the induction and maintenance of the inflammatory process. The skin, the nervous system and immunity are not independent systems but are closely associated and use the same language of cytokines and neurotransmitters. A new concept is suggested: the neuroimmunocutaneous system.
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PMID:Skin, immunity and the nervous system. 947 Aug 98

The vascular effects of endogenous substances can be easily studied in the skin. Early in this century, vasoregulation was shown to be dependent on innervation. Peptidergic transmitters have been shown to co-exist and co-transmit along with nonadrenalin and acetylcholine, sometimes being responsible for nonadrenergic-noncholinergic responses. This review summarizes recent information on vasoregulatory effects of neuropeptides such as substance P (SP), neurokinin A (NKA), calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase activating peptide (PACAP), neuropeptide Y (NPY), and somatostatin. All these peptides are vasodilators, and some of them seem to be involved in neurogenic inflammation. Some vasoactive peptides and other vasoactive molecules, such as nitric oxide (NO) and histamine, can originate both from nerves and cells and are crucially involved in vasoregulation. Other cell-derived peptides and molecules, such as bradykinin, endothelins, and prostaglandins, may contribute to neurogenic inflammation. All the peptides and molecules described also exist in other organs such as the brain, heart, lung, pancreas, and gastrointestinal tract. The effect of neuropeptides seems to vary from one organ or tissue to another, e.g., NPY is a potent vasoconstrictor in cardiac and cerebral vascular beds but acts as a vasodilator when it occurs in the skin. The presence of mast cells and inflammatory cells may create a special environment in the skin.
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PMID:Vasoactive peptides in the skin. 948 16

Nociceptin (20 microg/kg i.p.) strongly inhibited cutaneous Evans blue accumulation in the chronically denervated hindpaw of the rat in response to mast cell degranulating peptide (MCDP, 0.25 microg in 100 microl) but it had no and marginal effect on plasma extravasation induced by 5-hydroxytryptamine (5-HT, 0.5 microg in 100 microl) and histamine (0.1 microg in 100 microl), respectively. Release of sensory neuropeptides such as substance P, calcitonin gene-related peptide (CGRP) and somatostatin from the rat isolated trachea in response to capsaicin (10(-8) M) or bradykinin (10(-7) M) were also attenuated by nociceptin (100 and 300 nM). It is concluded that chemically induced discharge of mediators from mast cells and from capsaicin-sensitive afferent nerve terminals are both inhibited by nociceptin that participates in the anti-inflammatory effect of the peptide.
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PMID:Inhibition of nociceptin on sensory neuropeptide release and mast cell-mediated plasma extravasation in rats. 965 Aug 54

The effects of intra- and extra-adrenal peptides on [3H]dopamine uptake in adrenal chromaffin cells of the mouse were examined in vitro. Dopamine uptake was inhibited by acetylcholine, high potassium, reserpine, imipramine and desmethylimipramine as was in noradrenaline uptake. Among the intra-adrenal peptides, vasoactive intestinal peptide (VIP, 100 pmol/l) and neurotensin inhibited [3H]dopamine uptake by approximately 25%. Somatostatin, enkephalin, and neuropeptide Y did not cause any significant inhibition. An extra-adrenal peptide, bradykinin, inhibited the uptake while angiotensin II showed no significant effect. Intra-adrenal peptides which cause catecholamine secretion inhibit catecholamine uptake probably to extend its effect. Extra-adrenal peptide which causes catecholamine secretion also inhibits catecholamine uptake.
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PMID:Uptake of [3H]dopamine in isolated chromaffin cells of the mouse: modulation by intra- and extra-adrenal peptides and other secretagogues. 969 77

The aim of the present study was to analyze the neurochemical properties of the centrifugal visual system (CVS) of the quail using an immunohistochemical approach by testing 16 neuropeptides (angiotensin: ANG, bradykinin: BK, cholecystokinin, dynorphin, L and M-enkephalin, beta-endorphin: beta-END, galanin, alpha-neoendorphin, neurokinin A, neuropeptide Y (NPY), ocytocin, somatostatin, substance P, vasopressin, vasoactive intestinal polypeptide) and three neurotransmitters or their synthetic enzymes (choline acetyltransferase: ChAT, tyrosine hydroxylase: TH, serotonin: 5-HT and nitric oxide synthase: NOS, including the histochemical nicotinamide adenine dinucleotide phosphate diaphorase technique). For each substance, the somatic and afferent fiber and terminal labeling was analyzed within the nucleus isthmo-opticus (NIO) and the ectopic area (EA) and compared with that of retinopetal cell bodies labeled retrogradely with RITC following its intraocular injection (double-labeling procedure). The results showed that none of the centrifugal neurons were reactive to any of the substances tested. In contrast, all with the exception of ANG, BK and beta-END, labeled fibers and terminals within the EA and only four (ChAT, 5-HT, NPY and NOS) within the NIO. Possible sources of these immunoreactive fibers terminating in the NIO and EA were investigated by mapping the somatic immunolabeling of the different substances within brainstem regions previously shown by Miceli and other authors to project upon the centrifugal neurons. The data suggests that, besides the rapid retino-tecto-NIO-retinal loop, which facilitates the transfer of meaningful or more relevant information within particular portions of the visual field, the multiple afferent input which stems from various brainstem regions utilizes a wide range of neuroactive substances. Some of these afferent projections upon the centrifugal neurons appear to belong to nonspecific systems which might play a role in modulating the excitability of centrifugal neurons as a function of arousal.
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PMID:An immunohistochemical study of putative neuromodulators and transmitters in the centrifugal visual system of the quail (Coturnix japonica). 971 61


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