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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The role of circulating bradykinin in blood pressure regulation was studied in conscious spontaneously hypertensive rats utilizing the competitive antagonist of bradykinin B4162.2. This antagonist was administered at a bolus dose (400 μg i.v.) known to block the hypotensive effect of exogenous bradykinin for at least 2 min. The rats were maintained for 10 days either on a low or a high sodium intake.3. The antagonist of bradykinin significantly increased blood pressure only in salt- depleted rats. In other rats kept on a low or a high sodium intake, dose-response curves to exogenous bradykinin were established. Dietary sodium had no influence on the blood pressure-lowering effect of bradykinin.4. These data therefore suggest that circulating bradykinin may be involved in the blood pressure control of spontaneously hypertensive rats when the renin-angiotensin system is stimulated by salt depletion.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 652-655 
    ISSN: 1432-1912
    Keywords: Pain ; Kinins ; Receptor ; Inflammation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effect of bradykinin (BK) and some analogues of BK on the human blister base was studied. 2. BK produced reproducible dose-related increases in pain responses. A characteristic delay, which was not dose-related occurred between application of BK and the resultant response. 3. The rank order of potency of several kinin analogues on the pain response was BK 〉 〉 〉 Σ-cyclo-(Lys1-Gly6)-BK = Σ-cyclo-kallidin 〉 des-Arg9-BK. 4. No increase in pain response was seen with repeated application of the selective B1 receptor agonist des-Arg9-BK to the same blister base at 4 h intervals. The B1 receptor antagonist des-Arg9-Leu8-BK was without effect against BK-induced responses. 5. The B2 receptor antagonists, d-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-d-Phe-Thi-Arg-TFA and d-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride. 6. It is concluded that the kinin receptor mediating pain on the human blister base is of the B2 type.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-069X
    Keywords: Algogenic ; Bradykinin ; Bradykinin analogs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bradykinin has long been postulated to have a major role in physiologic human pain production. We have developed a method to systematically quantify the algogenic response to bradykinin in human skin by the direct application of bradykinin to suction blister bases. After determination of the pain threshold to bradykinin, we examined the ability of synthetic peptide analogs of bradykinin to block bradykinin-induced pain. One of the six analogs (B4642) inhibited bradykinin-induced pain with at least one concentration in all subjects tested. This result could not be predicted on the basis of inhibition of bradykinin binding to its guinea-pig ileum receptor or to previous studies of bradykinin-induced pain production in animal models. This peptide may have an eventual role as a physiologic pain inhibitor.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 430-433 
    ISSN: 1432-1912
    Keywords: Kinins ; Kinin antagonists ; Receptors ; Vascular permeability ; Inflammation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A range of bradykinin (BK) analogues was assessed for their ability to antagonise the action of BK on rabbit jugular vein, a B2-receptor containing tissue, and compared with their action against BK-induced increases in skin vascular permeability in the rabbit and rat. The results demonstrate that modification of the BK (nonapeptide) structure by the insertion of certain d-amino acids in positions 5, 7 and 8 in addition to elongation of the amino terminal resulted in compounds with potent antagonistic action against BK on rabbit jugular vein and rabbit skin vascular permeability. The same BK analogues did not antagonise the action of BK on rat skin vascular permeability. It is concluded that the kinin receptor mediating an increase in vascular permeability in the rabbit is the same as that mediating contraction of the rabbit jugular vein in vitro, that is the B2-type. The kinin receptor mediating an increase in skin vascular permeability in the rat is difficult to classify but does not appear to be of the B2 type.
    Type of Medium: Electronic Resource
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