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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 189-194 
    ISSN: 1432-1912
    Keywords: Substance P ; Phospholipids ; Cations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The partition of substance P (SP) between buffer solutions (pH 1.6–7.8) and an organic, phospholipid (phosphatidyl serine, phosphatidyl ethanolamine, phosphatidyl inositol and phosphatidyl choline) containing phase (chloroform:methanol 2:1) was studied. 2. The binding of SP to phosphatidyl serine, phosphatidyl ethanolamine and phosphatidyl inositol was lowest at pH 2 and increased with pH. The binding to phosphatidyl choline was much smaller and less dependent on pH. 3. In contrast to the basic peptide SP (pI 10.5), physalaemin (pI 7.0) did not show any binding to phospholipids at any investigated pH value which underlines the importance of a basic group in the peptide for its binding. 4. The high affinity (K D =0.1 μM) and capacity of 44 pmol SP/μg phosphatidyl serine and 48 pmol SP/μg phosphatidyl ethanolamine at pH 7.2 under conditions of saturation contrasted with the very low binding of SP to phosphatidyl inositol or phosphatidyl choline. Ionic bindings between the basic peptide and phosphatidyl serine or phosphatidyl ethanolamine are regarded to be predominant, although other binding forces cannot be excluded. 5. There was a concentration-dependent reduction in the binding of SP to phosphatidyl serine or phosphatidyl ethanolamine by Na+ and Ca2+, whereas K+ showed hardly any effect at physiological concentrations. 6. The model studies served to consider the possibilities of the binding of a basic peptide to lipid storage or receptor sites.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 310 (1979), S. 175-183 
    ISSN: 1432-1912
    Keywords: Substance P ; Antidromic vasodilation ; Neurogenic plasma extravasation ; Chemosensitive pain fibres ; Histamine ; Mast cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Antidromic vasodilation and neurogenic plasma extravasation were induced by antidromic stimulation of the saphenous nerve in guanethidine-treated rats. Vasodilation was measured by the change of outflow from the femoral vein and plasma extravasation was determined by Evans blue exudation. 2. Antidromic vasodilation was reduced by 85% in adult rats which were pretreated with capsaicin on the second day of life. 3. Antidromic vasodilation was inhibited by 46% after pretreatment with cimetidine plus mepyramine and by 64% after pretreatment with compound 48/80, but was not affected by pretreatment with cimetidine, atropine, methysergide, or indomethacin. Similarly, neurogenic plasma extravasation was reduced by 50% after pretreatment with cimetidine plus mepyramine, and by 88% after pretreatment with compound 48/80, but was not altered after pretreatment with indomethacin. 4. Infusion of substance P into the femoral artery dose-dependently produced vasodilation (threshold: 0.1 pmol min−1) and plasma extravasation (threshold: 0.5 pmol·min−1). Vasodilation induced by substance P was inhibited by 47% after pretreatment with cimetidine plus mepyramine and by 58% after pretreatment with compound 48/80. Plasma extravasation induced by substance P was reduced by 61% after pretreatment with cimetidine plus mepyramine and by 81% after pretreatment with compound 48/80. Pretreatment with indomethacin had no influence on substance P-induced vasodilation and plasma extravasation. 5. It is concluded that vasodilation and plasma extravasation following antidromic stimulation of sensory nerves are initiated by peripheral release of substance P from chemosensitive pain fibres. The actions of substance P include, besides direct effects, release of histamine from mast cells.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 311 (1980), S. 151-157 
    ISSN: 1432-1912
    Keywords: Substance P-binding ; Synaptic vesicles ; Regional distribution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Binding of 125I-Tyr8-substance P (SP) to synaptic vesicles shows an uneven distribution within the brain and the spinal cord. The regional distribution has a positive correlation with the SP-content, except in the hypothalamus. 2. Ca2+ and Mg2+-ions (1 and 10 mM) decrease the number of binding sites without alteration of affinity. EDTA and EGTA enhance SP-binding which is interpreted as being due to removal of the inhibitory influence of endogenous Ca2+ and Mg2+ through chelation with these agents. No significant inhibition of SP binding was observed by Na+ or K+ in concentrations below 100 mM. 3. Pretreatment of synaptic vesicles with trypsin or with phospholipase A2, C and D leads to a total loss of SP binding showing a proteolipid or a joint protein-phospholipid nature of these binding sites. SH groups do not contribute to SP binding since no effect of N-ethylmaleimide and monoiodoacetic acid on SP binding was found.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 165-171 
    ISSN: 1432-1912
    Keywords: Reactive hyperemia ; Substance P ; Vasoactive intestinal polypeptide ; Neurotensin ; Histamine ; Capsaicin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The cutaneous vasodilation following arterial occulusion (“reactive hyperemia”) was studied in the rat hind paw. A peak increase in venous outflow of 200–250% was observed within 1 min after a 3 min occlusion period. 2. Chronic denervation as well as capsaicin pretreatment reduced the postocclusive cutaneous vasodilatation by more than 60% (P〈0.01). This demonstrates that the reactive vasodilatation is of neurogenic origin and mediated by small diameter afferent fibres. 3. Reduction of the postocclusive cutaneous vasodilatation after histamine depletion by compound 48/80 indicates the involvement of histamine. 4. Among all neuropeptides known to occur in primary sensory neurones only substance P and vasoactive intestinal polypeptide cause vasodilatation when infused i.a. into the rat paw. In contrast to antidromic sensory nerve stimulation or i.a. substance P infusion, vasoactive intestinal polypeptide does not cause plasma extravasation. The vasodilator potency of vasoactive intestinal polypeptide is about 1/500 of substance P in the rat paw. Therefore only substance P is able to mimic the reactive vasodilatation. 5. It is concluded that the postocclusive cutaneous vasodilatation is caused mainly by the release of substance P from peripheral endings of small diameter nerve fibres. The “axon reflex”, also involving neurogenic vasodilatation, is assumed to be exerted by the same mechanism.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 240-243 
    ISSN: 1432-1912
    Keywords: Substance P ; Capsaicin ; Chronic denervation ; Neurogenic plasma extravasation ; Chemosensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Changes in the content of substance P (dorsal spinal cord, dorsal roots, dorsal root ganglia, saphenous nerve, skin) and functional changes (neurogenic plasma extravasation, chemosensitivity of the cornea) were measured in the rat from 10 min to 4 days after the s.c. injection of a single dose of 50 mg kg−1 capsaicin. 2. The substance P content in dorsal roots, saphenous nerve and hind paw skin progressively declined to about 60–70% of control 4 days after treatment, whereas that of the dorsal root ganglia rose, after an initial decline, to 140% after 1–4 days. 3. After denervation, impairment of neurogenic plasma extravasation could be observed not earlier than after one day, thus being comparable in time course to the depletion of substance P in the skin and saphenous nerve. 4. Neurogenic plasma extravasation and the chemosensitivity of the cornea were greatly diminished already 10 min after systemic capsaicin treatment, i.e. at a time when the substance P content of the peripheral nerve was still unchanged. These early effects of systemic capsaicin treatment are therefore caused by actions other than depletion of substance P.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1912
    Keywords: Substance P ; Somatostatin ; Neurotensin ; Capsaicin ; Sensory neurons ; Chemogenic pain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The distribution of immunoreactive substance P (I-SP), somatostatin (I-SRIF), and neurotensin (I-NT) and the effect of capsaicin treatment on the concentration of these peptides was studied in the peripheral and central nervous system of the rat. Neonatal capsaicin treatment (50 mg/kg s.c.) caused a depletion of I-SRIF as well as of I-SP in sensory nerves and in the dorsal half of the spinal cord. No recovery of the peptide content was found when examined 4 months later suggesting an irrerersible effect. I-NT, not a constituent of primary sensory neurons, was not changed in the spinal cord. None of the peptides studied was depleted in the hypothalamus or preoptic area. Capsaicin treatment of adult rats also led to a decrease of I-SRIF and I-SP in primarh sensory neurons. The highest dose used (950 mg/kg s.c.) induced no greater depletion than the lowest one (50 mg/kg), except for I-SP in dorsal root ganglia. Intraperitoneal injection of capsaicin led to a higher degree of depletion than subcutaneous administration as examined 1 week after treatment. In contrast to neonatal treatment, the I-SRIF content was completely restored within 4 months after treatment of adult rats. The I-SP content, however, did not completely recover in all areas but remained reduced in cornea, vagus nerve, dorsal spinal cord, and medulla oblongata for up to 9 months. Intraventricular administration of capsaicin (200 μg) caused a depletion of I-SP in the medulla oblongata but had no effect on the content of all 3 peptides in hypothalamus or preoptic area. In contrast to systemic treatment, no depletion of I-SP or I-SRIF was found in the trigeminal ganglion. Chemosensitivity of the eye was abolished after intraventricular or systemic treatment. Repeated topical application of a capsaicin solution (10 mg/ml) to the eye led within 4 h to a nearly complete depletion of I-SP in the cornea. These experiments show that capsaicin treatment of rats caused a depletion of both I-SRIF and I-SP in primary sensory neurons. While topical or systemic capsaicin administration causes depletion in terminals, the failure of intraventricular injections of capsaicin to deplete the peptides in the trigeminal ganglion suggests that depletion of the entire neuron requires an action of capsaicin on the peripheral branch and/or the cell body.
    Type of Medium: Electronic Resource
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