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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Synergism between the contractile effects of platelet-derived serotonin (5HT) and thromboxane A2 (TXA2) on a human blood vessel has been investigated by incubating strips of digital arteries in subcontractile concentrations of either 5HT or the TXA2-mimetic agent U46619.2. Either agonist U46619 or 5HT, in subcontractile concentrations, significantly potentiated the contractile response to the other.3. The 5HT antagonist ketanserin (10 (μmol/1), theCa2+ antagonist drugs verapamil (3 μmol/l), or nifedipine (10 nmol/l), or a Ca2+-free bathing medium, reduced the contractile responses to 5HT, but had no effect on the potentiation mediated by U46619.4. The interaction between TXA2 and 5HT derived from platelets was studied by measuring responses to platelets 1 min after aggregation (in the absence or the presence of ketanserin 10 μmol/l), and 20 min after aggregation. The results indicated that the response to platelets mediated by TXA2 and 5HT was greater than the sum of those mediated by TXA2 or 5HT separately.5. It is concluded that synergism between the contractile effects of 5HT and U46619 occurs in human blood vessels; that this is mediated by enhanced utilization of intracellular, rather than extracellular calcium; and that synergism can also occur when 5HT and TXA2 are released from stimulated human platelets.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 10 (1983), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The supernatant solutions obtained after aggregation or sonication of washed human platelets were superfused over preparations of human isolated digital arteries using a small volume bioassay method. The agents released from the platelets caused strong contractions of the artery strips.2. Platelet aggregation induced by 10 μg/ml collagen or by 100 μg/ml heat aggregated IgG, released 31.5% and 38.5% respectively, of the contractile activity produced by sonication of the platelets.3. The quantitative contractile effect of supernatants from platelets aggregated by 50 μg/ml IgG was significantly less than that for 100 μg/ml HA IgG. Similarly, the maximum contractile effect of supernatants from platelets aggregated by 300 ng/ml collagen was significantly less than that for 1 μg/ml collagen. This suggests that the concentration of contractile agents released from platelets depends on the concentration of aggregating stimulus.4. Comparison with concentration-effect curves for exogenous serotonin suggests that if the contractility of the platelet supernatant occurring after sonication of platelets is solely due to serotonin, then it is present in a concentration of approximately 3.3 times 10-6 mol/1 (6.6 nmol per 109 platelets).5. It is suggested from this study that in certain clinical situations characterized by hypertension, and in which circulating immune complexes have been found, in vivo platelet activation by immune complexes may be releasing sufficient concentrations of serotonin to constrict peripheral blood vessels and contribute to the hypertension.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The aim of these experiments was to determine if the vasorelaxation of the rat isolated aorta induced by sufentanil or alfentanil is mediated by the endothelium, and, if not, by α-adrenoceptor blockade, or a direct effect on the smooth muscle.2. Both sufentanil (from 10−7 mol/L to 10−4 mol/ L) and alfentanil (from 10−7 mol/ L to 3 × 10−4 mol/L) relaxed rings, where endothelium was intact and precontracted with 40 mmol/L KC1, in a concentration-related manner. Similarly, sufentanil and alfentanil relaxed rings, in the presence or absence of endothelium, which had been precontracted with phenylephrine.3. Naloxone (10−4 mol/L) had no significant effect on the relaxation induced by either sufentanil or alfentanil.4. In a similar manner as phentolamine, pretreatment with sufentanil protected α-adrenoceptors from blockade by phenoxybenzamine (PBZ) in both endothelium intact and denuded rings, but the estimated potency of sufentanil was approximately 100-fold less than that of phentolamine in α-adrenoceptor protection. Treatment with alfentanil did not produce any receptor protection.5. We concluded that, in the rat aorta, vascular relaxation induced by sufentanil is mediated by both α-adrenoceptor blockade and a direct effect on smooth muscle, whilst the relaxant effect of alfentanil is caused by direct effects alone. We also concluded that the endothelium has little role in relaxation produced by either drug.
    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 10 (1983), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Circulating immune complexes in excess of the equivalent of 20 m̈g/ml heat-aggregated IgG were found in fourteen out of twenty patients diagnosed as having preeclampsia.2. Only six of the nineteen controls tested had similar levels of immune complexes. Recent studies have established that concentrations of heat aggregated IgG in excess of 20 m̈g/ml activate human platelets to release sufficient concentrations of vasoactive agents to constrict a human blood vessel in vitro.3. It is therefore suggested that in vivo platelet activation by circulating immune complexes may release sufficient concentrations of vasoactive agents to contribute to the hypertension in pre-eclampsia.
    Type of Medium: Electronic Resource
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