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)

High levels of BN/GRP are present in classic SCLC and lung carcinoids, whereas BN immunoreactivity is absent in variant SCLC, adenocarcinoma, large cell carcinoma, squamous cell carcinoma, and mesothelioma cell lines. BN-like peptides are secreted from classic SCLC into the tissue culture medium. The secretion rate of BN-like peptides from cell line NCI-H345 was increased 3-fold by VIP (1 microM). Also, VIP increased the cAMP levels in cell line NCI-H345 by an order of magnitude. Therefore, SCLC cells have functional VIP receptors which regulate the secretion of BN-like peptides. Also, SRIF (100 nM) inhibits the VIP-stimulated increase in cAMP levels and secretion rate of BN-like peptides from SCLC cells. Because BN stimulates colony formation, VIP and/or SRIF may be able to alter the growth of SCLC cells. BN-like peptides are secreted from SCLC cells into the plasma. The levels of BN immunoreactivity in the plasma of SCLC patients with extensive disease is 2- to 40-fold greater than that of patients with limited disease. Secretin infusion into patients with extensive disease produces a transient increase (7-fold) in the plasma concentration of BN-like peptides. BN-like peptides are also present in the CSF of SCLC patients. When released from SCLC cells, BN-like peptides may interact with cell surface receptors. [Tyr4]BN binds with high affinity (Kd = 0.5 nM) to a single class of sites (1500/cell) on cell line NCI-H345. The carboxyl terminus of BN or GRP is essential for high-affinity binding activity. BN-like peptides elevate cytosolic Ca2+ levels as a result of increased phosphatidylinositol turnover. The putative BN receptor antagonist [D-Arg1, D-Pro2, D-Trp7,9, Leu11]substance P inhibits high-affinity [Tyr4]BN binding, the ability of BN to elevate cytosolic Ca2+ levels, and colony formation of SCLC cells. Therefore, BN receptor antagonists may serve as useful agents to inhibit the growth of SCLC.
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PMID:The release of bombesin-like peptides from small cell lung cancer cells. 285 97

[125I-Tyr]Somatostatin [( 125I-Tyr]SRIH) binding was found in 11 GH-secreting pituitary adenomas [Kd = 0.46 +/- 0.15 (+/- SE) nM; maximum binding, 165 +/- 35 fmol/mg protein). This binding was specific, since it was displaced by somatostatin-14 (SRIH-14), N-Tyr-SRIH-14, and SRIH-28. In contrast, a number of peptides and drugs not structurally related to SRIH, such as bombesin, dopamine, LHRH, met-enkephalin, naloxone, neurotensin, secretin, substance P, TRH, or vasoactive intestinal peptide, did not affect [125I-Tyr]SRIH binding. [125I-Tyr]SRIH specific binding also was found in PRL-secreting pituitary adenomas. The kinetic characteristics of the specific binding were similar to those of GH-secreting adenomas. However, maximal binding was one quarter that of GH-secreting adenomas (37 +/- 9 fmol/mg protein). In contrast, nonsecreting (chromophobe) tumors were devoid of any specific binding. Finally, in acromegaly, the density of [125I-Tyr]SRIH-binding sites in the adenomas was negatively correlated with plasma GH levels before surgery (r = -0.80). This suggests that somatostatinergic control is involved in GH secretion in acromegalic patients.
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PMID:Somatostatin receptors in human growth hormone and prolactin-secreting pituitary adenomas. 286 Jan 20

Somatostatin-like immunoreactivity (SLI) has been found throughout the gastrointestinal tract in all species examined. In the stomach it is mainly present in endocrine-type D-cells whereas in the intestine there is also an extensive distribution in enteric neurones. In all regions of the gastrointestinal tract multiple forms of somatostatin exist. A precursor (prosomatostatin) has been partially sequenced, three forms with 20 (SS-20), 25 (SS-25) and 28 (SS-28) amino acids completely sequenced, and somatostatin-14 (SS-14) demonstrated by radioimmunoassay. Both SS-14 and SS-28 exert a wide range of actions on the gastrointestinal tract and there is strong supportive evidence for a role in the regulation of gastric acid and gastrin secretion, gastrointestinal motility and intestinal transport. Both in vivo and in vitro studies on the secretion of gastric SLI into the vasculature have shown that nutrients initiate the process but that subsequent events are regulated by a complex interplay between hormonal and neuronal pathways. GIP is one of the most potent hormonal secretagogues. In the stomach, acetylcholine, opioid peptides and substance P are probably involved in parasympathetic inhibitory pathways and gastrin releasing peptide in stimulatory pathways. The sympathetic nerves are also stimulatory. Regulation of secretion of intestinal SLI has not been so extensively studied. Although SLI is also found in the gastrointestinal lumen the significance is unclear. Despite these advances the exact route of delivery of somatostatin to its target organs is uncertain and paracrine, endocrine and neural pathways may all be involved.
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PMID:Gastrointestinal somatostatin: distribution, secretion and physiological significance. 286 34

Vasodilation, conjunctival and nasal edema as well as miosis are symptoms associated with cluster headache (CH) attacks. Similar symptomatology is caused by substance P (SP) release from peripheral trigeminal nerve endings. The symptomatic effect of somatostatin (SRIF) during CH attacks was attributed to the inhibition of SP release from trigeminal neurons. This study was designed to evaluate both the vascular effect of SRIF on the dorsal hand vein and SRIF plasma levels prior to and after subcutaneous and intranasal administration in CH patients. A powerful venoconstriction and tachyphylaxis were demonstrated when SRIF was administered both as bolus and infusion. Plasma levels of SRIF in CH sufferers were lower than in control subjects. Subcutaneous and intranasal SRIF administrations induced maximal plasma levels after 5 and 10 min, respectively. These data suggest that SRIF plays an important role during CH attacks; however, its exact mechanism of action is still to be defined.
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PMID:A pharmacological approach to the analgesizing mechanism of somatostatin in cluster headache. 288 82

Functional and specific receptors for vasoactive intestinal peptide (VIP) (determined by their capacity to bind 125I-VIP and activate adenylate cyclase) and cyclic AMP-dependent phosphodiesterase activities were characterized in enterocytes of human fetal small intestine between 18 and 23 weeks of gestation. Half-maximal stimulation of the cyclase and inhibition of 125I-VIP binding in membrane preparations were respectively observed at 1.4 and 5 X 10(-10) M VIP. The peptides structurally related to VIP activated the cyclic AMP generating system at pharmacological doses (10(-7) M and above) in the following order of potency: VIP greater than PHI greater than GRF greater than secretin. Other peptides or test substances, including GIP, pancreatic glucagon, somatostatin-14, gastrin, CCK, neurotensin, pancreatic polypeptide, PYY, substance P, histamine and isoproterenol are inactive in this system, while the ubiquitous adenylate cyclase activators NaF, forskolin and prostaglandins were effective. These results, combined with the appearance of intestinal VIP in nerve fibers at 8 weeks and with the morphological and enzymatic maturation at 9-12 weeks of the intestinal mucosa, indicate that this neuropeptide may regulate either the differentiation or function of enterocytes during the early development of human intestinal mucosa.
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PMID:Vasoactive intestinal peptide receptor activity in human fetal enterocytes. 298 18

[125I]Iodo-Tyr1-somatostatin (SRIF) binds with high affinity to one class of sites in the rat anterior pituitary with a KD of 0.91 +/- 0.22 nM and a receptor concentration of 104.4 +/- 1.9 fmol/mg protein. This binding is saturable with respect to tissue concentration and is time-, temperature-, pH-, and calcium-dependent. It is also reversible as a function of time. The rates of association and dissociation were calculated to be 5.98 X 10(7) M-1 min-1 and 0.578 min-1, respectively. Binding of [125I]iodo-Tyr1-SRIF is not inhibited by morphine, beta-endorphin, [D-Ala2]Met-enkephalin, LHRH, TRH, histidylproline diketopiperazine, neurotensin, substance P, bombesin or vasoactive intestinal peptide. In contrast SRIF, [Tyr1]SRIF, and [D-Trp8,D-Cys14]SRIF displace [125I]iodo-Tyr1-SRIF binding with Ki values 0.10 +/- 0.05, 0.46 +/- 0.18, 0.05 +/- 0.01 nM, respectively. The constants of inhibition of a series of alanine monosubstituted analogs of SRIF are correlated (r = 0.89) with their biological potency on GH secretion. Furthermore, postnatal development patterns of [125I]iodo-Tyr1-SRIF binding sites follow the ability of SRIF to inhibit GH release. Thus, [125I]iodo-Tyr1-SRIF binding to adenohypophyseal membranes seems to reflect interaction with SRIF receptors on adenohypophyseal cells. Since biological effects of the peptide have been reported on GH, thyrotropin-stimulating hormone, and PRL secretion, further studies are required to determine the cell types upon which this binding occurs.
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PMID:Somatostatin receptors on rat anterior pituitary membranes. 612 57

To clarify whether various neuropeptides found in the hypothalamus act directly on a pituitary adenoma causing Nelson's syndrome, we examined the influence of these peptides on the secretion of immunoreactive ACTH, beta-endorphin, and melanotropins, the proopiomelanocortin (POMC)-derived peptides, by the cultured pituitary adenoma from a patient with Nelson's syndrome. Results showed that somatostatin-14 and somatostatin-28 suppressed the secretion of POMC-derived peptides by the adenoma and that somatostatin-28 was as potent as somatostatin-14. Other neuropeptides such as arginine vasopressin, vasoactive intestinal polypeptide, and oxytocin stimulate the secretion of POMC-derived peptides. Substance P, TRF, Met-enkephalin and Leu-enkephalin were also found to modulate the secretion of POMC-derived peptides. This suggests that the adenoma may have multiple receptors to various neuropeptides.
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PMID:Effects of various neuropeptides on the secretion of proopiomelanocortin-derived peptides by a cultured pituitary adenoma causing Nelson's syndrome. 612 87

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

Release of immunoreactive somatostatin (I-SRIF) and immunoreactive substance P (I-SP) was studied from slices prepared from upper dorsal horn (UDH) and lower dorsal plus ventral horn (LDH-VH) of rat spinal cord. Superfusion with capsaicin (10 microM) led to release of I-SRIF and I-SP from UDH slices but not from LDH-VH slices. The capsaicin-evoked release of I-SP was 6 fold higher than that of I-SRIF. A pulse of 60 mM K+ applied after the capsaicin pulse caused release of I-SRIF and I-SP from UDH as well as LDH-VH slices. Pretreatment of rats with capsaicin (125 mg/kg, s.c.) led to a nearly 40% depletion of I-SP in slices from UDH only. Capsaicin-evoked release from these slices was reduced by 81% for I-SRIF and by 79% for I-SP. Release evoked by K+ remained unchanged. These results indicate that capsaicin causes release of both I-SRIF and-I-SP and that this release is most likely restricted to primary sensory neurons. The marked reduction of the release of I-SP after systemic capsaicin pretreatment may well represent one of the, or even the reason for the insensitivity of capsaicin pretreated rats towards chemogenic pain.
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PMID:Effect of capsaicin pretreatment on capsaicin-evoked release of immunoreactive somatostatin and substance P from primary sensory neurons. 616 21

The amygdalofugal substance P (SP) and somatostatin (SRIF) neuron systems in the stria terminalis (ST) were investigated by means of the indirect immunofluorescence technique of Coons. SP- and SRIF-positive cells were mainly located in the area (Amc) between the central (ac) and medial (am) amygdaloid nuclei. Some extended medially into the am and laterally into the ac. Destruction of the Amc resulted in a marked reduction of SP- and SRIF-positive fibers in the ST. Furthermore, a substantial decrease in SP-positive fibers was seen in the dorsal part of the bed nucleus of the ST (stb), there was a small decrease in the SP-positive fibers in the lateral hypothalamus (LH), a significant decrease in the SRIF-positive fibers in the lateroventral part of the anterior hypothalamic nucleus (lvAH), and a small decrease in the SRIF-positive fibers in the LH. These facts indicate that the origins of a number of SP- and SRIF-positive fibers are the Amc and that the amygdalofugal SP pathway in the ST innervates stb and LH and the amygdalofugal SRIF pathway in the ST projects to lvAH and LH.
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PMID:Experimental immunohistochemical studies on the amygdalofugal peptidergic (substance P and somatostatin) fibers in the stria terminalis of the rat. 616 92


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