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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    The effect of chronic ethanol administration on nitric oxide-mediated responses in rat isolated trachea preparation (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 In the present study, we investigated the effect of chronic ethanol administration on nitric oxide (NO)-mediated responses in rat isolated trachea preparation. 2 Ethanol was given to rats in a modified liquid diet for 21 days. Isolated tracheal rings were then used to obtain responses to electrical field stimulation (EFS) after precontraction with 100 μm histamine. The parameters of field stimulation were as follows: supramaximal voltage of 50 V, 0.5 ms duration, 10-s train; 0.5, 1, 3, 5, 10, 20, 30 and 50 Hz at 2-min intervals. The effects of l-and d-arginine (10−6 m) on the responses to field stimulation (10–20 Hz) were studied. In other experiments, we tested the effects of Nω-nitro-l-arginine methyl ester (l-NAME, 10−6–10−5 m) and SIN-1 (10−6–10−5 m) on the responses to field stimulation. 3 Electrical field stimulation induced relaxation responses in the tracheal rings precontracted with histamine from control- and ethanol-treated rats. The relaxation responses induced by EFS were significantly reduced in the tracheal rings precontracted with histamine from ethanol dependent group. The responses induced by EFS in both groups were completely abolished by tetrodotoxin (1 μm), but unaffected by hexamethonium (1 μm). Incubation with d-arginine did not cause statistically significant increases in relaxation responses to EFS in both groups. l-Arginine (10−6 m) caused statistically significant increases in relaxation responses to EFS in control rats, but not in ethanol dependent rats. Incubation with l-NAME (10−6–10−5 m) caused statistically significant inhibition of the relaxation responses to EFS in both groups. SIN-1 (10−6–10−5 m) induced significantly increase in relaxation responses to EFS in both groups. 4 Our results suggest that the possible mechanism responsible for inhibition of tracheal inhibitory responses to EFS in ethanol-dependent rats may be a reduction in production of NO and in the uptake of l-arginine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00281.x
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of nitric oxide synthase blockade on responses to morphine in rat aortic rings (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 It has been suggested that opioids may play an indirect role in the regulation of the peripheral circulation through the control of nitric oxide (NO) release in vascular tissue. The current study was undertaken to investigate the effect of nitric oxide synthase (NOS) blockade on responses to morphine in phenylephrine (PE)- or KCl-precontracted rat aortic rings. 2 Morphine (3 × 10−8−3 × 10−5 m) administration did not cause any significant effect on basal tonus of endothelium-intact or endothelium-denuded preparations. Morphine produced concentration-dependent relaxation responses in endothelium-intact as well as in endothelium-denuded rat aortic rings precontracted by PE or KCl. Removal of endothelium did not significantly alter the relaxation responses to morphine. 3 The relaxant responses to morphine were significantly and partially inhibited by pretreatment of tissues with naloxone (NAL, 3 × 10−5 m) for 5 min. The inhibitory effect of NAL on relaxant responses to morphine in PE- or KCl-precontracted rings did not differ significantly between endothelium-intact and endothelium-denuded preparations. 4 Incubation of endothelium-intact or endothelium-denuded rat aortic rings with NOS inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME, 10−4 m) for 20 min did not cause a significant inhibition on relaxation responses to morphine. 5 These findings confirmed the presence of opiate receptors in rat thoracic aorta, but suggested that mechanisms other than NO release play a role in the relaxant effect of morphine on rat aortic rings.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2002.00249.x
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