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  • Articles  (91,334)
  • 2000-2004  (91,334)
  • 2003  (91,334)
  • Chemistry and Pharmacology  (84,342)
  • Electrical Engineering, Measurement and Control Technology  (7,587)
  • Education  (553)
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  • Articles  (91,334)
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  • 2000-2004  (91,334)
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  • 1
    Electronic Resource
    Electronic Resource
    11th Meeting on Adrenergic Mechanisms: Porto, Portugal 25–27 September 2003.
Noradrenaline transporter knockout-mediated regulation of serotonin receptors in mice brain (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
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00307.x
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  • 2
    Electronic Resource
    Electronic Resource
    Alpha2-adrenoceptor and NO mediate the opioid subsensitivity in isolated tissues of cholestatic animals (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 Our previous report showed that in acute cholestasis, the subsensitivity to morphine inhibitory effect on electrical-stimulated contractions develops significantly faster in guinea-pig ileum (GPI) and in mouse vas deferens (MVD) (45.2 and 29.9 times, respectively) compared with non-cholestatic subjects. 2 The possible contribution of α2-adrenoceptor and nitric oxide (NO) pathways on the development of tolerance was assessed in GPI and MVD of cholestatic subjects. 3 Daily administration of naltrexone (20 mg kg−1), yohimbine (5 mg kg−1), and Nω-nitro-l-arginine methyl ester (l-NAME) (3 mg kg−1) to cholestatic animals significantly (P-value 〈 0.05) inhibited the process of subsensitivity in all groups. 4 Consistent with the literature, it was concluded that both the α2-adrenergic system and NO have close interaction with the opioid system and may underlie some of the mechanisms involved in the subsensitivity development to opioids in acute cholestatic states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00297.x
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  • 3
    Electronic Resource
    Electronic Resource
    NO/cyclic GMP pathway mediates the relaxation of feline lower oesophageal sphincter (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 We examined the role of the NO/cyclic GMP (cyclic GMP) pathway in nitric oxide (NO)- and vasoactive intestinal peptide (VIP)-induced relaxation of feline lower oesophageal sphincter (LES). Furthermore, it was studied whether methylene blue, LY83583 and ODQ, which are soluble guanylate cyclase (sGC) inhibitors, could inhibit NO-induced relaxation.2 The nitric oxide synthase (NOS) inhibitor, N-nitro-l-arginine (l-NNA) had no effect in sodium nitropruside (SNP)-induced relaxation, but 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1)-induced relaxation was decreased by the pretreatment of l-NNA, which showed that SIN-1, not SNP, could activate NOS to cause relaxation. Methylene blue and LY83583 did not inhibit the relaxation by SNP and SIN-1. However, the more specific sGC inhibitor ODQ blocked the relaxation induced by NO donors.3 To identify the relationship of NOS, sGC and adenylate cyclase in VIP-induced relaxation, tissue were pretreated with l-NNA and ODQ and SQ22536. These inhibitors produced significant inhibition of this response to VIP. The adenylyl cyclase inhibitor SQ 22536 also inhibited relaxation by VIP.4 In conclusion, our data showed that SNP- and SIN-1-induced relaxation was mediated by sGC. Of sGC inhibitors, methylene blue and LY83583 were not adequate for the examination of NO donor-induced feline LES smooth muscle relaxation. VIP also caused relaxation by the pathway involving NO and cGMP and cAMP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00291.x
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  • 4
    Electronic Resource
    Electronic Resource
    Mechanisms of release of ATP from vascular purinergic nerves (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 vasoconstrictor response to periarterial nerve electrical stimulation (PNS) and neurotransmission by ATP are discussed and illustrated, using canine isolated and perfused splenic arterial preparations. 2 The conditions for appearance of dominant purinergic constrictor response to PNS are discussed. 3 Modulation of the purinergic vasoconstrictor responses to PNS by several kinds of presynaptic receptor agonists and antagonists is reviewed. 4 Influences of purinergic responses to PNS by guanethidine, reserpine, tetrodotoxin (TTX) or ω-conotoxin GVIA (ωCTX) are also reviewed. 5 Effects of imipramine and removal of the endothelium are discussed. 6 Evidence is presented for selective inhibition of purinergic responses to PNS by an adequate cold storage of the vessel. 7 The roles of ATP released by PNS in isolated canine splenic arteries are proposed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00283.x
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  • 5
    Electronic Resource
    Electronic Resource
    The effects of selective phosphodiesterase III and V inhibitors on adrenergic and non-adrenergic, non-cholinergic relaxation responses of guinea-pig pulmonary arteries (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 aim of the present study was to investigate the role of several possible neurotransmitters in mediating non-adrenergic, non-cholinergic (NANC) relaxation, and the effects of phosphodiesterase (PDE) III and V inhibitors on adrenergic and NANC relaxation in branch pulmonary artery (PA) of guinea-pig. 2 Under the NANC conditions, electrical field stimulation (EFS, 60 V, 0.2 ms, 20 Hz) induced a tetrodotoxin-sensitive relaxation of the histamine-precontracted PA rings. The nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10−4 m) and the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10−5 m) partially inhibited the EFS-induced relaxation. The inhibitory effect of l-NAME was reversed completely by l-arginine (10−3 m), but not d-arginine (10−3 m). 3 This NANC relaxation was attenuated by 8-phenyltheophylline (10−5 m), a P1-purinoceptor antagonist. 4 The NANC response was potentiated by 10−6 m zaprinast, a type V PDE inhibitor, but was unaffected by 3 × 10−6 m milrinone, a type III PDE inhibitor. 5 Sodium nitroprusside (SNP) caused a concentration-dependent vasodilator effect which was potentiated by zaprinast, but unaffected by milrinone. Moreover, the effect of combination of zaprinast with milrinone was not significantly different from that observed with zaprinast alone. 6 Isoprenaline produced a concentration-dependent vasodilatation in branch PA of guinea-pig which was potentiated by both zaprinast and milrinone, the efficacy of milrinone being greater than zaprinast. 7 These results suggest that both nitrergic and purinergic pathways are involved in mediating the NANC relaxation in branch PA of guinea-pig. The combination of PDE III or V inhibitors with vasorelaxant drugs may be a hopeful approach for the treatment of pulmonary hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00284.x
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  • 6
    Electronic Resource
    Electronic Resource
    Author index (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
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2003.00310.x
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  • 7
    Electronic Resource
    Electronic Resource
    AT1-receptor blockade and sympathetic neurotransmission in cardiovascular disease (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 survey is dealing with the interactions between the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system (SNS) in various organs and tissues, with an emphasis on the angiotensin AT-receptors located at the sympathetic nerve endings. 2 Angiotensin II, the main effector of the RAAS is known to stimulate sympathetic nerve traffic and its sequelae in numerous organs and tissues, such as the central nervous system, the adrenal medulla, the sympathetic ganglia and the sympathetic nerve endings. These stimulatory effects are mediated by AT1-receptors and counteracted by AT1-receptor antagonists. 3 Sympatho-inhibition at the level of the sympathetic nerve ending appears to be a class effect of the AT1-receptor blockers, mediated by presynaptic AT1-receptors. With respect to the ratio pre-/postsynaptic AT1-receptor antagonism important quantitative differences between the various compounds were found. 4 Both the pre- and postjunctional receptors at the sympathetic nerve endings belong to the AT1-receptor population. However, the presynaptic receptors belong to the AT1B-subtype, whereas the postjunctional receptors probably belong to a different AT1-receptor subpopulation. 5 Sympatho-inhibition is a class effect of the AT1-receptor antagonists. In conditions in which the SNS plays a pathophysiological role, such as hypertension and congestive heart failure, this property may well be of therapeutic relevance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00301.x
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  • 8
    Electronic Resource
    Electronic Resource
    Coronary and aortic vasoconstriction by cathinone, the active constituent of khat (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 psychostimulant constituent of khat leaves, S-(−)-cathinone, was examined for vascular activity on the coronary vasculature of guinea-pig-isolated perfused hearts and aortic ring preparations. 2 Cathinone caused coronary vasoconstriction, negative inotropy and negative chronotropy in isolated hearts. The major metabolite of cathinone after its ingestion, 1R.2S-(−)-norephedrine (norephedrine), also caused coronary vasoconstriction comparable with that by cathinone. Norephedrine, however, had no effect on force or rate of cardiac contractions. 3 Cocaine (10 μm) potentiated the coronary vasoconstriction and positive inotropy by noradrenaline indicating inhibition of neuronal uptake. The vasoconstriction and negative inotropy by cathinone, however, were not affected, indicating that its action was not via release of noradrenaline from sympathetic neurones. 4 The α1-adrenoceptor antagonist, prazosin, blocked the vasoconstriction by noradrenaline, but not that produced by cathinone in the presence of cocaine. This indicates that the coronary vasoconstriction by cathinone was not due to an action on α1-adrenoceptors either directly or indirectly through noradrenaline release. 5 Three repeated doses of cathinone displayed the same coronary vasoconstrictor responses, indicating a lack of tachyphylaxis and therefore confirming that the response was unlikely to be due to indirect sympathomimetic activity through release of noradrenaline. 6 In guinea-pig aortic rings, the order of vasoconstrictor activity was: noradrenaline 〉 norephedrine 〉 cathinone, with each causing approximately equivalent maximum responses. The time to reach plateau contractions was shortest for noradrenaline (5.1 ± 0.5 min), then norephedrine (9.3 ± 1.5 min) and cathinone the longest (25.4 ± 3.2 min, 335 μm dose). 7 These results indicate that cathinone has vasoconstrictor activity which is not due to indirect or direct sympathomimetic activity. The precise mechanism for this vasoconstriction remains to be determined. The coronary vasoconstriction may explain the increased incidence of myocardial infarction in khat chewers, which may arise from coronary vasospasm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00303.x
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  • 9
    Electronic Resource
    Electronic Resource
    Prostanoid-induced modulation of neuropeptide Y and noradrenaline release from the rat mesenteric bed (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 A variety of prostanoids were examined for their ability to alter the periarterial nerve stimulation-induced release of noradrenaline (NA) and neuropeptide Y immunoreactive compounds (NPY-ir) from the perfused mesenteric arterial bed of the rat. 2 Periarterial nerve stimulation (16 Hz) increased the overflow of NA, NPY-ir and perfusion pressure. 3 The prostacyclin (PGI2) analogues, carbaPGI2 and cicaprost both produced a concentration-dependent attenuation of the nerve stimulation-induced increase in NA, NPY-ir overflow and perfusion pressure. 4 The prostaglandin (PG) analogue PGE2 attenuated the evoked increase in NPY-ir overflow as well as a modest decrease in NA. 5 PGE1, sulprostone and iloprost attenuated the nerve stimulation-induced increase in NA overflow but not NPY-ir. 6 Neither PGF2α nor the thromboxane A2 analogue U46619 altered the evoked increase in NA or NPY-ir overflow. 7 The results support the view that sympathetic co-transmitter release can be differentially modulated by paracrine/autocrine mediators at sympathetic neuroeffector junctions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00288.x
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  • 10
    Electronic Resource
    Electronic Resource
    Rilmenidine produces mydriasis in cats by stimulation of CNS α2-adrenoceptors (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 Experiments were undertaken to determine if the imidazoline/α2-adrenoceptor agonist, rilmenidine, would produce mydriasis in cats and, if so, to delineate its site of action and determine if this effect is mediated by imidazoline receptors or α2-adrenoceptors. 2 Rilmenidine produced dose-related pupillary dilator responses in pentobarbital anaesthetized cats that were independent of sympathetic innervation to the iris but were dependent upon intact parasympathetic neuronal tone. The ED50 for rilmenidine-induced pupillary dilation was approximately 200 μg kg−1, i.v., and was sustained for at least 1 h. 3 The highly selective α2-adrenoceptor antagonist, RS-79948, administered either before or after rilmenidine, antagonized rilmenidine-induced mydriasis. Neuronally induced reflex inhibition of parasympathetic nerve activity was also inhibited by administration of RS-79948. 4 These results suggest that rilmenidine acts like clonidine to produce pupillary dilation by inhibition of parasympathetic tone to the iris sphincter and that this central nervous system parasympatho-inhibition is mediated by α2-adrenoceptors, rather than imidazoline receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00276.x
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