Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Receptors for porcine vasoactive intestinal peptide have been characterized in isolated epithelial cells of rat ventral prostate. The interaction of 125I-labelled VIP with cells was rapid, reversible, specific, saturable and dependent on temperature. Degradation of peptide and receptors was minimized at 15 degrees C. At apparent equilibrium, the binding of 125I-labelled peptide was competitively inhibited by native VIP in the 1 X 10(-10)-10(-7)M range concentration. The binding data were compatible with the existence of two classes of receptors: a high-affinity class with a Kd = 4.0 nM and a low binding capacity (0.12 pmol VIP/mg cell protein), and a low-affinity class with a Kd = 17.8 nM and a high binding capacity (1.6 pmol VIP/mg cell protein). Chicken VIP and porcine secretin exhibited a 7-fold higher and a 7-fold lower affinity than porcine VIP for binding sites, respectively. Glucagon, Leu-enkephalin, Met-enkephalin and somatostatin were ineffective. The presence of high-affinity receptors for VIP together with previous reports on the occurrence of VIP-containing neurones innervating the male genitourinary tract strongly suggest that this peptide may be important in the physiological regulation of the functions of prostatic epithelium.
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PMID:Receptors for vasoactive intestinal peptide on isolated epithelial cells of rat ventral prostate. 631 51

Vasoactive intestinal peptide (VIP) has been shown to increase cyclic AMP content in isolated epithelial cells of rat ventral prostate. The stimulatory effect of VIP was dependent on time and temperature and was potentiated by a phosphodiesterase inhibitor. At 15 degrees C, the response occurred in the 1 X 10(-10)-10(-7)M range of VIP concentrations. Half-maximal stimulation of cellular cyclic AMP was obtained at 1.4 nM and maximal stimulation (3-fold basal level) at about 100 nM VIP. Chicken VIP and porcine secretin were agonists of porcine VIP but exhibited a 2-times higher and a 170-times lower potency, respectively. A high concentration (1 X 10(-6)M) of glucagon, somatostatin, neurotensin, substance P, Met-enkephalin or Leu-enkephalin did not modify cAMP levels. The finding of a VIP-stimulated cAMP system in rat prostatic epithelial cells together with the previous characterization of high-affinity receptors for VIP in the same cell preparation, as well as the presence of VIP-containing neurones innervating the male genitourinary tract, strongly suggest that VIP may be involved in prostatic growth regulation and function.
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PMID:Cyclic AMP-stimulating effect of vasoactive intestinal peptide in isolated epithelial cells of rat ventral prostate. 631 52

Plasma methionine-enkephalin-like and leucine-enkephalin-like immunoreactivity (met-enkephalin-LI and leu-enkephalin-LI, respectively) in six normal subjects and six patients with pheochromocytoma were determined. The contents of met-enkephalin-LI and leu-enkephalin-LI in two of six pheochromocytomas were 40- to 50-fold higher and those in the other four pheochromocytomas were less than those in normal human adrenal medulla. The former two patients showed high plasma met-enkephalin-LI and leu-enkephalin-LI levels. As plasma catecholamines levels returned to the normal range after extirpation of tumors, met-enkephalin-LI and leu-enkephalin-LI in plasma became undetectable in these patients. In contrast, neither met-enkephalin-LI nor leu-enkephalin-LI was detected in plasma from the latter four patients. Met-enkephalin-LI and leu-enkephalin-LI concentrations were higher in the adrenal vein than in the peripheral vein in three patients. Plasma met-enkephalin-LI and leu-enkephalin-LI increased concomitantly with catecholamines after glucagon stimulation and during a spontaneous attack in a patient with pheochromocytoma. Plasma met-enkephalin-LI changed in parallel with leu-enkephalin-LI in all cases. High performance liquid chromatography coupled with RIAs has shown that met-enkephalin and leu-enkephalin circulate in plasma from a patient with pheochromocytoma as intact pentapeptides. None of normal subjects showed detectable concentrations of met-enkephalin-LI and leu-enkephalin-LI in plasma (more than 5 pg/ml and 3 pg/ml, respectively). It is concluded that met-enkephalin and leu-enkephalin are released concomitantly with catecholamines from pheochromocytomas.
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PMID:Plasma methionine-enkephalin and leucine-enkephalin in normal subjects and patients with pheochromocytoma. 688 62

VIP stimulated prolactin secretion from incubated rat hemipituitaries. Under the same conditions, the secretion of GH, LH, FSH was not affected. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations whereas another partial analogue, glucagon, was ineffective. The effect of VIP was not blocked by alpha-flupentixol, a potent dopaminergic antagonist, at concentrations which antagonized the dopamine inhibition of prolactin secretion. Stimulation by VIP and TRH was additive. Neither Met-enkephalin nor naloxone interfered with the response to VIP. It thus seems that specific VIP receptors are present on pituitary prolactin cells. VIP, present in the mediobasal hypothalamus and detected in the hypothalamo-hypophyseal portal blood therefore is a good candidate as a physiological PRF.
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PMID:Stimulation of in vitro prolactin release by vasoactive intestinal peptide. 741 20

Because of the enormous growth over the last three decades of research on the role of peptides in the brain, the need became apparent to determine the status of these compounds in terms of their current research interest. Since 1965, over a quarter of a million research papers have been published on peptides that have since been classified as neuroactive. The present study was undertaken to analyze systematically the yearly trends of research emphasis in neuroactive peptides as reflected by their individual frequency of publication by year, beginning in 1966. A computer analysis of the publication characteristics was carried out using the Medline data base in which the citation search was limited to the topic brain crossed with the topic mammal. One criterion for the inclusion of a given peptide in the analysis was a frequency of 25 or more citations following its discovery, as related to the mammalian brain. The 42 peptides that met this criterion were: adrenocorticotropic hormone, angiotensin II, atrial natriuretic factor, bombesin, bradykinin, calcitonin, calcitonin gene-related peptide, carnosine, beta-casomorphin, cholecystokinin, corticotropin-releasing factor, delta sleep-inducing peptide, dynorphin, beta-endorphin, Leu-enkephalin, Met-enkephalin, galanin, gastrin, glucagon, growth hormone, growth hormone-releasing factor, insulin, kyotorphin, beta-lipotropin, luteinizing hormone-releasing factor, melanocyte-stimulating hormone release inhibitory factor-1, alpha-melanocyte-stimulating hormone, motilin, neurokinin A, neurokinin B, neuropeptide Y, neurotensin, oxytocin, pituitary adenylate cyclase activating polypeptide, peptide HI, prolactin, secretin, somatostatin, substance P, thyroid-releasing hormone, vasopressin, and vasoactive intestinal peptide. An overall analysis of the 298,105 papers published on these 42 peptides since 1965 revealed that the research activity of 24,742, or 8.30%, of the studies, focused on their neuroactive properties. Taken as a whole, the research on neuroactive peptides reached a peak in 1986, as reflected by the total of 1793 papers published during that year. Although the level of publication has fluctuated between 1548 and 1774 research papers over the last 6 years, it is now clear that the trend in research on neuroactive peptides has reached an asymptote today that shows no sign of deviation. A temporal analysis year by year of individual publication profiles revealed three distinct trends: 1) peptides showed a slow development in research interest and did not exceed more than 15-30 publications per year; 2) peptides exhibited a steady increase in research activity over the years that continues today; and 3) peptides displayed an initial, often intense, research emphasis that inexplicably declined, in some cases precipitously, in the mid 1980s.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuroactive peptides: unique phases in research on mammalian brain over three decades. 800 41

Group III and IV muscle afferents are active during exercise and relay information from mechano- and metaboreceptors in muscle. We hypothesized that these afferents participate in the regulation of endocrine and metabolic adjustments to exercise. Muscle branches of the femoral nerves were electrically stimulated in 10 anesthetized and paralyzed cats at 3, 20, and 140 times motor threshold, for 10 min at each intensity, recruiting group III afferents at 20 times motor threshold and group III and IV afferents at 140 times motor threshold. Six cats were not stimulated but were otherwise treated as stimulated cats. [3-3H]glucose was infused intravenously, and arterial blood was sampled for analysis of substrates and hormones. Three times motor threshold stimulation induced no changes in measured metabolic parameters. Twenty times motor threshold stimulation elicited increases (P < 0.05 vs. control) in glucose production (8.2 +/- 1.8 mumol.min-1.kg-1) and plasma glucose (0.29 +/- 0.07 mmol/l) and adrenocorticotropic hormone (ACTH; 35 +/- 12 pg/ml). Stimulation at 140 times motor threshold elicited increases (P < 0.05 vs. control) in glucose production (10.2 +/- 5.4 mumol.min-1.kg-1), plasma glucose (0.53 +/- 0.10 mmol/l), ACTH (94 +/- 28 pg/ml), beta-endorphin (17 +/- 6 pg/ml), and Met-enkephalin (15 +/- 2 pg/ml) and decreases (P < 0.05 vs. control) in insulin (0.65 +/- 0.14 microU/ml). Glycerol and glucagon did not change with stimulations. The findings provide evidence for a reflex control from muscle of hormone secretion and mobilization of glucose during exercise.
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PMID:Reflex control of glucoregulatory exercise responses by group III and IV muscle afferents. 816 Aug 77

A single, large dose of N-methyl-D-aspartate (NMDA) or quisqualic acid (QA) injected into the chick eye has been shown previously to destroy many retinal amacrine cells and to induce excessive ocular growth accompanied by myopia. The purpose of this study was to identify distinct populations of retinal cells, particularly those believed to be involved in regulating ocular growth, that are sensitive to NMDA or QA. Two pmol of NMDA or 0.2 micromol of QA were injected unilaterally into eyes of 7-day-old chicks, and retinas were prepared for observation 1, 3, or 7 days later. Retinal neurons were identified by using immunocytochemistry, and cells containing fragmented DNA were identified by 3'-nick-end labelling in frozen sections. NMDA and QA destroyed many amacrine cells, including those immunoreactive for vasoactive intestinal polypeptide, Met-enkephalin, and choline acetyltransferase, but they had little effect upon tyrosine hydroxylase-immunoreactive cells. Other cells affected by both QA and NMDA included those immunoreactive for glutamic acid decarboxylase, gamma-aminobutyric acid, parvalbumin, serotonin, and aminohydroxy methylisoxazole propionic acid (AMPA) receptor subunits GluR1 and GluR2/3. Cells largely unaffected by QA or NMDA included bipolar cells immunoreactive for protein kinase C (alpha and beta isoforms) and amacrine cells immunoreactive for glucagon. DNA fragmentation was detected maximally in many amacrine cells and in some bipolar cells 1 day after exposure to QA or NMDA. We propose that excitotoxicity caused by QA and NMDA induces apoptosis in specific populations of amacrine cells and that these actions are responsible for the ocular growth-specific effects of QA and NMDA reported elsewhere.
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PMID:Immunocytochemical characterization of quisqualic acid- and N-methyl-D-aspartate-induced excitotoxicity in the retina of chicks. 952 96


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