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  • 1
    ISSN: 1432-0428
    Keywords: Keywords Amylin ; hypertension ; calcitonin ; ACE inhibition ; calcitonin gene related peptide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Amylin (or islet amyloid polypeptide) has been reported to have binding sites in the central nervous system and the kidney and has been shown to activate plasma renin. It has been postulated that this peptide may be an important mechanistic link between hypertension and diabetes in the insulin resistance syndrome. To explore this issue, the effects of rat amylin on mean arterial blood pressure were investigated in anaesthetised rats. Amylin elicited a pressor response of approximately 10 mmHg (maximal at 100 pmol · kg–1) which was apparent within 30–60 s and persisted over 15 min. At higher concentrations amylin elicited a hypotensive response (negative log IC50 8.52 mol · kg–1). The novel amylin receptor antagonist AC413 (12 nmol · kg–1· min–1) reduced the pressor response but not the hypotensive effects of amylin. The peptide antagonist calcitonin gene-related peptide (CGRP)8–37 (12 nmol · kg–1· min–1) reduced the pressor response elicited by amylin and also antagonized the hypotensive effect of amylin. Pre-treatment of animals with the ganglion blocker mecamylamine (3 mg · kg–1 s. c.) reduced the pressor effect of amylin. Following the administration of the angiotensin converting enzyme inhibitor ramiprilat (300 nmol · kg–1 i. v.) the pressor response to amylin was reduced. Salmon calcitonin also elevated blood pressure in the anaesthetised rat; doses of amylin and salmon calcitonin associated with a pressor effect were associated with increases in plasma renin activity. We conclude that amylin may act centrally to elevate blood pressure in the anaesthetised rat, possibly through activation of the renin angiotensin system. [Diabetologia (1997) 40: 256–261]
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 117 (1926), S. 342-343 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] DURING the great East Anglian herring fishery which takes place during October, November, and part of December, almost all of the fish taken are either spawning or are in the condition which just precedes spawning. It has been shown that the main areas in which eggs are deposited are near ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 24 (2004), S. 0 
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 The great taxonomic and prey base diversity of colubrids (non-front-fanged snakes) suggests that their venoms may represent a ‘literal gold mine’ for scientists eager to find novel pharmacological probes (Mackessy, 2002). 2 While pharmacological characterization is lacking for most of these venoms, this is even more so with regard to activity of colubrid venoms on the mammalian autonomic nervous system. This study characterizes the activity of venom from the colubrid, Boiga dendrophila using in vitro smooth muscle preparations and the anaesthetized rat. 3 In the prostatic segment of the rat vas deferens, cumulative additions of venom (1–150 μg ml−1) induced concentration-dependent inhibition of electrically evoked (0.2 Hz, 0.3 ms, 70–100 V) twitches. The inhibitory effect of venom (100 μg ml−1) was attenuated by 8-phenyltheophylline (8-PT) (20 μm) and 8-cyclopentyl-1, 3-dipropylxanthine (20 μm) but not idazoxan (1 μm), or a combination of ranitidine (0.2 μm) and thioperamide (10 μm). The inhibitory effect of venom (100 μg ml−1) was augmented by dipyridamole (10 μm) but abolished by pretreatment with adenosine deaminase (7.5 units/100 μl) suggesting that it contains components with adenosine A1 receptor activity, most likely adenosine. 4 In isolated segments of guinea-pig ileum, venom (10–100 μg ml−1) caused concentration-dependent contractions which were inhibited by the muscarinic receptor antagonist atropine (0.1 μm) but not by the histamine receptor antagonist mepyramine (0.5 μm). 5 In the anaesthetized rat, venom (5–7.5 mg kg−1, i.v.) caused a hypotensive effect. 6 Our data suggest that the venom contains components with purinergic and muscarinic receptor activity.
    Type of Medium: Electronic Resource
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  • 4
    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: SUMMARY1. Arachidonic acid (AA, 0.125–1.0 mg/kg) injected via the aorta into the autoperfused hindquarters caused dose-dependent increases in perfusion pressure. This effect was reduced after intravenous administration of the thromboxane receptor antagonist AH23848 (5 mg/kg) or indomethacin (5 mg/kg).2. Responses to AA (0.125–1.0 mg/kg) were reduced markedly in the Krebs-perfused hindquarters when compared with those occurring in the blood-perfused preparation.3. Doses of guanethidine (1 mg/kg) and pentacynium (1 mg/kg) blocking pressor responses to intravenous administration of the ganglion stimulants McN-A-343 and DMPP, respectively, did not affect responses to AA.4. Constrictor responses to AA (0.5–1.0 mg/kg) in blood-perfused hindquarters were increased in 14 day alloxan-diabetic rats but those to the thromboxane A2-mimetic U46619 (0.5–8.0 μg/kg, i.a.) were reduced when compared with non-diabetic controls.5. In 14 day alloxan-diabetic rats vasoconstrictor responses to noradrenaline and methoxamine were potentiated but those to 5-hydroxytryptamine were reduced compared with non-diabetic animals.6. It is concluded that AA causes constriction in the blood-perfused hindquarters by release of a product of cyclo-oxygenase acting on thromboxane A2-receptors. A constituent of blood, perhaps the platelet, appears necessary for this effect. Conversion of AA to the constrictor metabolite is augmented during experimentally induced diabetes.
    Type of Medium: Electronic Resource
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