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 effects of tetraethylammonium (TEA), a K+ channel antagonist, on vasodilator responses were investigated in the hindquarters vascular bed of the cat under constant-flow conditions. After administration of TEA in a total dose of 60 mg/kg into the hindquarters perfusion circuit, vasodilator responses to acetylcholine, bradykinin, and substance P were reduced, whereas vasodilator responses to the NO donors, diethylamine-NO complex, S-nitroso-N-acetylpenicillamine, and sodium nitroprusside, and to prostaglandin E1, albuterol, vasoactive intestinal polypeptide, isradipine, and levcromakalim were not altered. The inhibitory effect of TEA on responses to the endothelium-dependent vasodilators was reversible with time, and vasoconstrictor responses to norepinephrine, U-46619, angiotensin II, and BAY K 8644 were enhanced by the K+ channel antagonist. Although TEA had no sustained effect on baseline systemic arterial and hindquarters perfusion pressures, the NO synthase inhibitor, N omega-nitro-L-arginine methyl ester, increased these pressures in the presence of TEA. The results of the present investigation suggest that TEA attenuates vasodilator responses to acetylcholine, bradykinin, and substance P by inhibiting the release of endothelium-derived relaxing factor. These data suggest that the acetylcholine-, bradykinin-, and substance P-stimulated release of endothelium-derived relaxing factor may involve the opening of a TEA-sensitive K+ channel in the endothelium in the hindlimb vascular bed of the cat, but that a TEA-sensitive mechanism is not involved in the maintenance of baseline tone in this vascular bed.
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PMID:Vasodilator responses to acetylcholine, bradykinin, and substance P are mediated by a TEA-sensitive mechanism. 924 80

Trefoil peptides are a family of small proteins expressed by goblet cells that are secreted onto the apical gastrointestinal mucosal surface, where they are present in high concentrations. These peptides appear to both protect the epithelium and promote healing after injury. However, the factors regulating the expression and secretion of these proteins contributing to mucosal defense have not been characterized. To determine the mechanisms controlling production of trefoil peptides, the human colon cancer-derived model cell line HT-29 was exposed to a variety of potential secretagogues. Expression and secretion of human intestinal trefoil factor (hITF) as well as the intestinal apomucin MUC2 were assessed by Northern and Western blot analysis. Carbachol, an analog of acetylcholine, and the neuroendocrine peptides somatostatin and vasoactive intestinal polypeptide (VIP) stimulated increased expression of hITF mRNA within 5 min. These same factors stimulated parallel secretion of the hITF peptide, with maximal stimulation observed at concentrations ranging from 10(-6) M (carbachol and somatostatin) to 10(-7) M (VIP). Expression and secretion of hITF in response to carbachol, VIP, and somatostatin was independent of production of apomucin. hITF was not regulated by other neuroendocrine transmitters including histamine and substance P. Similarly, hITF expression and secretion was not modulated by peptide growth factors (epidermal growth factor, transforming growth factor-beta, and keratinocyte growth factor), cytokines [interleukin (IL)-1 beta, IL-2, IL-7, and IL-11], or arachidonic acid metabolites (prostaglandin E1/E2 and leukotriene B4). In conclusion, trefoil peptides appear to be integrated into mechanisms of mucosal defense and repair through the enteric neuroendocrine system and independent of the classical mucosal immune cytokine network.
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PMID:Trefoil peptide expression and secretion is regulated by neuropeptides and acetylcholine. 927 13

Rat parotid salivary gland acinar cells were transfected by CaPO4 precipitation using a plasmid containing a replication-defective simian virus (SV40) genome. Out of 30 clonal cell lines, 2 were shown to have moderate to high levels of cytodifferentiation and salivary gland acinar cell function. Functional studies with the two cell lines indicated that the beta-adrenergic agonist (isoproterenol), vasoactive intestinal peptide prostaglandin E1, and forskolin were effective activators of intracellular cyclic adenosine 3':5'-cyclic monophosphate production. Phenylephrine, carbamylcholine, and UTP were effective in increasing inositol phosphate production and intracellular free calcium levels, whereas substance P was without affect. Utilizing indirect immunofluorescence analysis, both cell lines were shown to express the SV40 large T antigen. Electron microscopic evaluation documented moderate to high levels of cytodifferentiation with the maintenance of tripartite junctional complexes, cellular polarization, and presence of moderate amounts of secretory granules and rough endoplasmic reticulum. The two cell lines had doubling times of 22 and 36 h, respectively.
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PMID:Development and characterization of SV40 immortalized rat parotid acinar cell lines. 954 37

The purpose of this investigation was to develop well-differentiated rat parotid and submandibular acinar cell lines. Acinar cells dissociated from rat parotid and submandibular glands were grown on Mitomycin C-treated 3T3 fibroblasts or Matrigel in primary culture and transfected by CaPO4 precipitation using a plasmid containing a replication-defective simian virus (SV40) genome. Cytokeratin analysis via indirect immunofluorescence and receptor mediated changes in intracellular calcium and cyclic AMP were assessed and used for the identification and selection of immortalized epithelial cells. Of the more than 60 clonal cell lines, four retained moderate to high levels of acinar differentiation through >60 passages. Ultrastructurally, there were tripartate junctional complexes and moderate amounts of rough endoplasmic reticulum and secretory granules. Functional studies indicated that beta-adrenoceptors, vasoactive intestinal peptide, and prostaglandin E1 were effective activators of intracellular cyclic AMP production in all cell lines. Alpha-adrenoceptors, muscarinic cholinoceptors, and P2U-purinoceptor agonists were effective in increasing intracellular inositol phosphate production and free calcium levels whereas substance P was ineffective. These data document the utility of the SV40 plasmid in immortalizing rat parotid and submandibular acinar cells that retain most of the features of acinar differentiation.
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PMID:Development and characterization of immortalized rat parotid and submandibular acinar cell lines. 982 93

In the isolated guinea pig hearts suppression of endothelium-dependent (Acetylcholine, Substance P, postocclusive hyperaemia) and endothelium-independent (Sodium nitroprusside, PGE1) responses after 30 min subglobal ischaemia (reduction of coronary flow to 5%) were analysed in hearts which were not preconditioned or preconditioned by various protocols. Preconditioning consisted of single 5 min ischaemia (IP5) or single 10 min ischaemia (IP10) or double 5 min ischaemia (IP5 + 5). Thirty minutes of ischaemia followed by reperfusion reduced both endothelium-dependent and endothelium-independent responses approximately by 30-50% and slightly suppressed basal coronary flow by 10%. IP5 and IP5 + 5 protected against postischaemic suppression of responses to NaNP but not against postischaemic impairment of SP, ACh, and POH responses. The endothelium-dependent responses and postischaemic suppression of basal coronary flow were protected by IP10 only. In summary, in the isolated guinea pig heart the 30-min ischaemia impairs vasodilator responses to both endothelium-dependent and endothelium-independent agents. Ischaemic preconditioning protects both endothelial and smooth muscle cells function against this impairment, though endothelial cells require a more extensive preconditioning to put in motion protective mechanisms than smooth muscle cells do. Independent mechanisms of IP in endothelial cells and in smooth muscle cells are suggested.
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PMID:Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning. 1063 11


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