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  • Articles  (231,564)
  • 2000-2004  (231,564)
  • Medicine  (231,564)
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  • Articles  (231,564)
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  • 1
    Electronic Resource
    Electronic Resource
    Author index (2004)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 24 (2004), 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.1474-8673.2004.00326.x
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  • 2
    Electronic Resource
    Electronic Resource
    Differential effects of FK506 and cyclosporin A on catecholamine release from bovine adrenal chromaffin cells (2004)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 24 (2004), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 The effects of the immunosuppressants, tacrolimus (FK506) and cyclosporin A (CsA), on catecholamine (CA) release were examined in cultured bovine adrenal chromaffin cells. 2 In intact cells, FK506 (1–30 μm) inhibited CA release stimulated by acetylcholine (ACh; 100 μm), 1,1-dimethyl-4-phenyl-piperazinium (DMPP, 10 μm) or high K+ (40 mm). CsA (1–30 μm) had a little inhibitory effect on the ACh- or DMPP-stimulated CA release, whereas it enhanced the high K+-stimulated CA release. 3 In β-escin-permeabilized cells, FK506 inhibited CA release stimulated by Ca2+ (1 and 10 μm) in the presence and absence of MgATP (2 mm). CsA induced CA release under Ca2+-free condition and enhanced the Ca2+-stimulated CA release in the presence and absence of MgATP. 4 It is known that the Ca2+-dependent exocytosis involves at least two distinct steps, ATP-requiring priming stage and ATP-independent fusion step in adrenal chromaffin cells. Therefore, it is suggested that FK506 inhibits the Ca2+-dependent exocytosis probably at the fusion step whereas CsA induces CA release from bovine adrenal chromaffin cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00316.x
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  • 3
    Electronic Resource
    Electronic Resource
    Functional alterations of mesenteric vascular bed, vas deferens and intestinal tracts in a rat hindlimb unloading model of microgravity (2004)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 24 (2004), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 Prolonged bed rest or exposure to microgravity may cause several alterations in autonomic nervous system response (ANSR). 2 Hindlimb unloading (HU) rats were used as an animal model of simulated microgravity to investigate ANSR changes. The experiments were carried out to investigate the effects of simulated microgravity on the autonomic nervous response of the perfused mesenteric vascular bed (MVB), vas deferens and the colon and duodenum from 2-week HU rats. 3 In MVB preparations of HU rats, the frequency-dependent increases in perfusion pressure with perivascular nerve stimulation (PNS; 8–40 Hz) were inhibited, whereas the noradrenaline (NA) concentration-dependent (1–100 μm) perfusion pressure increases were potentiated. The latter most probably reflected up-regulation of α-adrenergic receptor function. Relaxant responses of NA-precontracted MVB to PNS (4–30 Hz) or isoprenaline were not different between control and HU preparations, while vasodilation induced by the endothelial agonist ACh was reduced. 4 Transmural stimulation (2–40 Hz) induced frequency-dependent twitches of the vas deferens which were reduced in vas deferens of HU rats, while the sensitivity to NA-induced contraction was significantly increased. 5 In the gastroenteric system of HU rat, direct contractile responses to carbachol or tachykinin as well as relaxant or contractile responses to nervous stimulation appeared unchanged both in the proximal colon rings and in duodenal longitudinal strips. 6 In conclusion, HU treatment affects peripheral tissues in which the main contractile mediators are the adrenergic ones such as resistance vessels and vas deferens, probably by reducing the release of neuromediator. This study validates NA signalling impairment as a widespread process in microgravity, which may most dramatically result in the clinical phenotype of orthostatic intolerance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00315.x
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of atipamezole — a selective α2-adrenoceptor antagonist — on cardiac parasympathetic regulation in human subjects (2004)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 24 (2004), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 This double-blind, cross-over, placebo-controlled study on six healthy male volunteers was designed to evaluate the effects of α2-adrenoceptor antagonism on cardiac parasympathetic regulation. 2 The subjects received atipamezole intravenously as a three-step infusion, which aimed at steady-state serum concentrations of 10, 30 and 90 ng ml−1 at 50-min intervals. 3 Drug effects were assessed with repeated recordings of blood pressure and electrocardiogram, in which the high-frequency (0.15–0.40 Hz) R-R interval variation is supposed to reflect cardiac parasympathetic efferent neuronal activity. 4 At the end of the three steps of the infusion, the mean (±SD) concentrations of atipamezole were 10.5 (3.9), 26.8 (5.6) and 81.3 (21.1) ng ml−1. 5 Within this concentration range, atipamezole appeared to reduce slightly the high-frequency R-R interval fluctuations, indicating a minor vagolytic effect in the heart. 6 Atipamezole increased systolic and diastolic arterial pressure, on average by 20 and 14 mmHg (maxima at the second step of the infusion), which evidently reflects an overall sympathetic augmentation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00318.x
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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
    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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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Histamine receptor type coupled to nitric oxide-induced relaxation of guinea-pig nasal mucosa (2002)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 22 (2002), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 The aim of this study was to characterize the histamine receptor type mediating relaxation of the vascular bed of the nasal mucosa from the guinea-pig, and to determine the role of cyclo-oxygenase products and nitric oxide in this relaxant response to histamine. These studies were performed in isolated nasal mucosae examined in vitro to obtain potencies of histamine receptor-type selective agonists in causing vasorelaxation and to determine affinities of histamine receptor antagonists for inhibiting histamine-induced relaxation. 2 After contraction of nasal mucosae with noradrenaline, histamine caused a maximal relaxation response that was 75 ± 6% of the contraction caused by noradrenaline with a mean EC50 value of 4.3 ± 0.5 μm. Neither dimaprit (H2-receptor selective) nor R-α-methylhistamine (H3-receptor selective) caused significant relaxation of nasal mucosae. In contrast, betahistine (H1-receptor selective) caused an 81 ± 7% relaxation of noradrenaline-induced tone with an EC50 value of 15 ± 1 μm. 3 pA2 experiments were performed to obtain KB values of chlorpheniramine (H1-receptor selective) and diphenhydramine (H1-receptor selective) for blocking histamine-stimulated relaxation of nasal mucosae. KB values for chlorpheniramine (0.87 nm) and diphenhydramine (7.4 nm) were consistent with their interaction at the H1-receptor type. Additionally, neither 10 μm cimetidine (H2-receptor selective) nor 1 μm thioperamide (H3-receptor selective) had any effect on the relaxation curve for histamine. 4 In the presence of 10 μm indomethacin (cyclo-oxygenase inhibitor), histamine caused a maximal relaxation response of 73 ± 5% of the noradrenaline-induced tone with an EC50 value of 2.9 ± 0.2 μm, which was not different from control values (EC50 = 5.0 ± 0.4 μm; maximal relaxation = 71 ± 6%). In contrast, 200 μm NG-nitro-l-arginine (nitric oxide synthase inhibitor) completely inhibited histamine-induced relaxation of nasal mucosae. 5 In conclusion, data from the present study suggest only the H1-receptor type mediates relaxation of nasal mucosal blood vessels to histamine, and histamine-induced relaxation of nasal mucosae is entirely dependent on nitric oxide production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2002.00268.x
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