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  • 1
    Electronic Resource
    Electronic Resource
    Increased blocking activity of combined tachykinin NK1- and NK2-receptor antagonists on tachykinergic bronchomotor responses in the guinea-pig (2003)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 23 (2003), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 The present study compared the effect of the administration of tachykinin NK1- and NK2-receptor antagonists alone and in combination on exogenous and endogenous tachykinin-induced contractions using three different guinea-pig airway preparations: isolated bronchus, isolated perfused lung and in vivo. 2 In the isolated bronchi, the tachykinin NK1-receptor antagonist CP 99994 (0.01–1 μm)produced concentration-dependent inhibition of contractions induced the tachykinin NK1-receptor agonists substance P (SP) and [Met-OMe11] SP ([Met-OMe11]SP), whereas the tachykinin NK2-receptor antagonist SR 48968 (0.1 μm) had no effect. SR 48968 (0.001–0.01 μm)concentration-dependently inhibited contractions induced by the tachykinin NK2-receptor agonists neurokinin A (NKA) and [β-Ala8]-neurokinin A (4–10) ([βAla8]-NKA) whereas CP 99994 (0.1 μm) did not inhibit the contractions. The contractile activity of capsaicin, an agent that releases endogenous tachykinins from sensory C-fibres, was inhibited in a concentration dependent manner by SR 48968 (0.001–0.03 μm) but not by CP 99994 (0.1 μm). Combination of CP 99994 and SR 48968 caused increased inhibitory effects on the concentration–response curves to SP, [Met-OMe11]SP, NKA, [β-Ala8]-NKA and capsaicin. 3 In isolated perfused lungs, SR 48968 concentration (0.01–10 μm) dependently inhibited NKA-, [β-Ala8]-NKA- and capsaicin-induced bronchoconstriction whereas CP 99994 (30 μm) had no effect on SP-, NKA-, [β-Ala8]-NKA- and capsaicin-induced bronchoconstriction. Combination of inactive concentrations of CP 99994 and SR 48968 produced an increased inhibitory effect on all previous stimuli-induced bronchoconstriction. 4 In in vivo guinea-pig studies, intravenous and oral pretreatment with SR 48968 (0.01–1 mg kg−1 i.v. and 0.1–3 mg kg−1 p.o., respectively), but not with CP 99994 (1 mg kg−1 i.v. and 0.3–30 mg kg−1 p.o., respectively), produced a dose-dependent inhibition of the bronchoconstrictor responses induced by NKA, [β-Ala8]-NKA and capsaicin. CP 99994 intravenously (0.3 mg kg−1) and orally (3–10 mg kg−1) inhibited SP-induced bronchoconstriction only. Intravenous and oral low dose combinations of CP 99994 and SR 48968 produced an increased inhibition of SP-, NKA-, [β-Ala8]-NKA- and capsaicin-induced bronchoconstriction, respectively. 5 The present data indicate that combined tachykinin NK1- and NK2-receptor antagonist treatment compared with single antagonist treatment, using CP 99994 and SR 48968, produced an augmented blockade of tachykinin NK1-, NK2- and capsaicin-mediated contractions in guinea pig airways. These findings support the hypothesis that a dual NK1- and NK2-receptor antagonist may provide an advantage over single activity tachykinin NK1- or NK2-receptor antagonists in pulmonary obstructive diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00279.x
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  • 2
    Electronic Resource
    Electronic Resource
    Pharmacological characterization of α2-adrenoceptor-mediated responses in pig nasal mucosa (2003)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 23 (2003), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 Pig nasal mucosal strips were incubated with α-adrenoceptor antagonists followed by α2-adrenoceptor agonist concentration–response curves. 2 Contractions elicited by the α2-adrenoceptor agonists BHT-920 (pD2 = 6.16 ± 0.07), UK 14,304 (pD2 = 6.89 ± 0.13) and PGE-6201204 (pD2 = 7.12 ± 0.21) were blocked by the α2-adrenoceptor antagonist yohimbine (0.1 μm). In contrast, the α1-adrenoceptor antagonist prazosin (0.03 μm) had no effect on the BHT-920-, UK 14,304- and PGE-6201204-induced contractions, but blocked the contractile response to the α1-adrenoceptor agonist phenylephrine (pD2 = 5.38 ± 0.04) and the mixed α1- and α2-adrenoceptor agonist oxymetazoline (pD2 = 6.30 ± 0.22). 3 The α2-adrenoceptor antagonist yohimbine (0.01–0.1 μm, pA2 = 8.04), α2B/C-adrenoceptor antagonist ARC 239 (10 μm, pKb = 6.33 ± 0.21), α2A/C-adrenoceptor antagonist WB 4101 (0.3 μm, pKb = 8.01 ± 0.24), α2A-adrenoceptor antagonists BRL44408 (0.1 μm, pKb = 6.82 ± 0.34) and RX 821002 (0.1 μm, pKb = 8.31 ± 0.35), α2C-adrenoceptor antagonists spiroxatrine (1 μm, pKb = 7.32 ± 0.32), rauwolscine (0.1 μm, pKb = 8.16 ± 0.14) and HV 723 (0.3 μm, pKb = 7.68 ± 0.14) inhibited BHT-920-induced contractions in pig nasal mucosa. 4 The present antagonist potencies showed correlations with binding affinity estimates (pKi) obtained for these antagonists at the human recombinant α2A- and α2C-adrenoceptors (r = 0.78 and 0.83, respectively) and with binding affinity estimates (pKd) obtained in pig native α2A- and α2C-monoreceptor assays (r = 0.85 and 0.78, respectively). No correlation was observed for the α2B-subtype. 5 In conclusion, contractile responses to phenylephrine, BHT-920, UK 14,304, PGE-6201204 and oxymetazoline indicate that α1- and α2-adrenoceptors are present and mediate vasoconstriction in pig nasal mucosa. Furthermore, correlation analysis comparing antagonist potency in pig nasal mucosa with affinities for human recombinant α2-adrenoceptors and native pig α2-adrenoceptors suggest that α2A- and α2C-adrenoceptor subtypes constrict pig nasal mucosa vasculature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2003.00298.x
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  • 3
    Electronic Resource
    Electronic Resource
    Antihistamine activity, central nervous system and cardiovascular profiles of histamine H1 antagonists: comparative studies with loratadine, terfenadine and sedating antihistamines in guinea-pigs (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Sedation limits the clinical utility of classical H, antihistamines. while newer antihistamincs such as loratadine and terfenadine arc non-sedating. However, clinical use of terfenadine has been associated with rare but severe cardiac arrhythmias, in particular lorsades de pointes.Objective To establish a quantitative experimental model for assessing the sedating and cardiotoxicity potential of non-sedating and sedating antihistamines.Methods Drugs were administered intravenously and the integrated amplitude of the conical electroencephalogram (EEC) signal was recorded. The threshold dose that depressed EEG activity was compared with the dose required lo inhibit by 50% the peripheral bronchospasm elicited by 10 μg/ kg i.v., of histamine. In separate studies, the electrocardiogram (ECG) and cardiovascular effects of loratadine (30 and 100mg/kg, i.v.). terfeuadine (10mg/kg. i.v.). promethazine (5mg/kg. i.v.) and diphenhydramine (20 mg kg, i.v.) were evaluated.Results The sedating antihistamines. diphenhydramine and promethazine. depressed the integrated EEG at doses between 0.6 and 2.0 limes their peripheral antihisiamine doses. Loratadine had no EEG depressant activity at 100 mg kg. i.v., a dose more than I 70 times its LD50 (0.58 mg kg, i.v.) against histamine bronchospasm. We were unable lo evaluate the EEG effects of terfenadine. because it produced cardiovascular collapse at 10 mg/kg. i.v. Loratadine and promethazinc did not produce adverse cardiovascular effects. nor did they alter normal ECG activity. Diphenhydramine produced brady-cardia followed by a transient hypertensive phase without affecting the QTc interval. In contrast, terfenadine elicited hypotension, bradycardia and significant arrhythmogenic activiy, causing a prolongation of the QTc interval and a torsades de pointes like ventricular arrhythmia. Pharmacokinetic studies after i.v. administration of loraladine (30 and 100 mg/kg) demonstrated plasma levels of loratadine and its major metabolite descarboethoxyloratadine to be several orders of magnitude greater than levels found in humans at the clinical dose of 10mg.Conclusion The CNS depressant effects of H1 antihislamines arc promcthazine≅ diphenhdramine ≫ loratadine = placebo. Of the non-sedating antihistamines. loratadine was devoid of adverse cardiovascular effects whereas terfenadine caused a pronounced disruption of the normal ECG. characterized by a torsades de pointes-like effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb00400.x
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  • 4
    Electronic Resource
    Electronic Resource
    Cardiovascular profile of loratadine (1999)
    Oxford BSL : Blackwell Science Ltd
    Clinical & experimental allergy 29 (1999), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The extremely low reporting rate of cardiovascular adverse events for loratadine, the possible preferential use of loratadine in patients with pre-existing cardiovascular disorders, and the impressive lack of cardiovascular effects at extremely high concentrations in clinical and preclinical studies demonstrate the very safe cardiovascular profile of loratadine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.1999.0290s3197.x
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  • 5
    Electronic Resource
    Electronic Resource
    Studies on the mechanism of clonidine-induced mydriasis in the rat (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1985), S. 258-263 
    Details
    ISSN: 1432-1912
    Keywords: Mydriasis ; Clonidine ; Yohimbine ; Monoamine depletion ; CNS ; Postsynaptic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Intravenous administration of clonidine hydrochloride (3–100μg/kg) produced a dose-dependent pupillary dilation in anaesthetized rats. All experiments were carried out in rats in which vagosympathetic nerve trunks were sectioned bilaterally at the cervical level. 2. Clonidine-induced mydriasis was present only in those preparations having intact parasympathetic neural tone to the iris. 3. Depletion of CNS monoamines by more than 95% with reserpine (5mg/kg) and alpha-methyl-para-tyrosine (2×300mg/kg) failed to alter the dose-response relation to clonidine. 4. Pretreatment with the alpha-2-adrenoceptor antagonist, yohimbine hydrochloride (1.5 mg/kg), produced about a 10-fold shift to the right in the pupillary dose-response curve to clonidine. Yohimbine administered after the highest dose of clonidine also antagonized the mydriatic response. 5. The above results suggest that clonidine acts on CNS post-synaptic alpha-2-adrenoceptors to produce mydriasis by withdrawal of parasympathetic neural tone to the iris. 6. In an attempt to assess the physiological substrate(s) involved, mydriatic responses, due to parasympatho-inhibition, were evoked by electrial stimulation of ascending (sciatic nerve and medullary) and descending (hypothalamic) pathways. 7. Yohimbine (0.3 and 1.0mg/kg) produced a dose-dependent inhibition of the pupillary dilation evoked by stimulation of the sciatic nerve and medullary loci, whereas these doses of yohimbine failed to alter the dilation in response to hypothalamic stimulation. 8. Similarly, monoamine depletion greatly antagonized the pupillary dilation elicited by sciatic nerve and medullary stimulation without significantly affecting mydriasis due to hypothalamic stimulation. 8. These results suggest that pupillary dilation produced by activation of ascending inhibitory mechanisms may utilize a monoamine as an inhibitory neurotransmitter (perhaps noradrenaline) and that inhibition descending from the hypothalamus is not monoaminergic. It is further speculated that clonidine may produce mydriasis in this species by activation of CNS post-synaptic alpha-2-adrenoceptors (perhaps on neurons of the Edinger-Westphal nucleus) which normally subserve tonic inhibition arising from the periphery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00515551
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  • 6
    Electronic Resource
    Electronic Resource
    Activation of histamine H3 receptors produces presynaptic inhibition of neurally evoked cat nictitating membrane responses in vivo (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 346 (1992), S. 208-212 
    Details
    ISSN: 1432-1912
    Keywords: Histamine H3 receptors ; Cat nictitating membrane ; (R)-α-Methylhistamine ; Thioperamide ; Presynaptic inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was undertaken in order to determine the potential role of prejunctional histamine H3 receptors in an in vivo adrenergic model system. Frequency-dependent nictitating membrane responses were elicited by sympathetic nerve stimulation in anesthetized cats. Systemic administration of the selective histamine H3 receptor agonist, (R)-α-methylhistamine (RαMeHA) produced a dose-related depression of amplitude of the evoked nictitating membrane responses with a threshold of about 10 μg/kg and maximal effect (50% depression at the lowest frequency; 0.5 Hz) seen at 100–300 gg/kg. Responses obtained with low frequency stimulation were more sensitive to depression by RaMeHA than were responses evoked with higher frequencies of stimulation. Larger doses of RaMeHA given to the same animals, failed to produce additional inhibition. RαMeHA depressed the amplitude of nictitating membrane responses evoked by either pre- or postganglionic nerve stimulation to an equivalent degree. This depressant action of RαMeHA was antagonized by pretreatment with the specific histamine H3 antagonist, thioperamide (3 mg/kg), but not by combined pretreatment with histamine H1 and H2 blockers chlorpheniramine (300 Ftg/kg) and cimetidine (5 mg/kg). Intravenous administration of adrenaline (1–30 wg/kg) also produced graded nictitating membrane responses that were not altered by subsequent administration of RαMeHA. These results suggest that histamine H3 receptors are involved in the modulation of neurally evoked noradrenaline release in the cat nictitating membrane by an inhibitory presynaptic action. The most likely site of drug action appears to be at the neuroeffector junction as no appreciable ganglionic effect of RαMeHA was observed in this in vivo model system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165303
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  • 7
    Electronic Resource
    Electronic Resource
    Prejunctional inhibition of sympathetically evoked pupillary dilation in cats by activation of histamine H3 receptors (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 141-145 
    Details
    ISSN: 1432-1912
    Keywords: Histamine H3 receptors ; Cat pupil ; (R)-α-Methylhistamine ; Thioperamide ; Presynaptic inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Frequency-dependent pupillary dilations were evoked by electrical stimulation of the pre- or post-ganglionic cervical sympathetic nerve (sympatho-excitation) or the hypothalamus (parasympatho-inhibition) in sympathectomized anesthetized cats. Systemic administration of the selective histamine H3 receptor agonist (R)-α-methylhistamine (RαMeHA) produced a dose-dependent depression of mydriasis due to direct neural sympathetic activation but had no effect on responses elicited by parasympathetic withdrawal. The histamine H2 receptor agonist, dimaprit, was inactive. RαMeHA was much more effective in depressing sympathetic responses obtained at lower frequencies when compared to higher frequencies of stimulation. Responses evoked both pre- and postganglionically were inhibited by RαMeHA. This peripheral sympathoinhibitory action of RαMeHA was antagonized by the histamine H3 receptor blocker thioperamide but not by intravenous pretreatment with the histamine H1 receptor antagonist chlorpheniramine. Histamine H2 receptor blockers cimetidine and ranitidine were also without effect. RαMeHA did not depress pupillary responses elicited by i.v. (-)-adrenaline. The results demonstrate that histamine H3 receptors modulate sympathetic activation of the iris at a site proximal to the iris dilator muscle. The predominant mechanism of action appears to the prejunctional inhibition of noradrenaline release from postganglionic sympathetic nerve endings. However, a concomitant ganglionic inhibitory action cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164790
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  • 8
    Electronic Resource
    Electronic Resource
    Perfluorinated membranes as catalyst supports (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Applied Organometallic Chemistry 4 (1990), S. 465-473 
    Details
    ISSN: 0268-2605
    Keywords: Perfluorinated membrane ; catalyst support ; metal particle catalysts ; metal complex catalysts ; hydrogenation ; isomerization ; Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: The perfluorinated polymer Nafion and porous PTFE/Nafion composite membranes have been employed as supports for nickel complexes or for platinum and palladium metal particles. The resultant materials have been employed as catalysts in various olefin conversion processes. Supported platinum and palladium metal systems were evaluated as catalysts for the hydrogenation of cyclohexene. Rates of reaction are better than those of commercially available catalysts; turnover numbers in excess of 6000 have been obtained with no poisoning apparent. Catalysts may be regenerated many times. The reduction rate approaches a limit at high pressures of hydrogen and has an activation energy of 13 kJ mol-1 in neat cyclohexene. Nafion was employed as a strong acid cocatalyst to activate and then support a nickel complex catalyst. The resultant catalyst was active for double-bond-shift isomerization.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aoc.590040507
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