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  • 1
    Electronic Resource
    Electronic Resource
    INVOLVEMENT OF ENDOTHELIAL CYCLO-OXYGENASE METABOLITES IN NORADRENALINE-INDUCED CONTRACTION OF RAT CORONARY ARTERY (2005)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Noradrenaline (NA; 0.3 µmol/L) caused a contraction of the rat coronary artery that markedly increased in the presence of the nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME; 100 µmol/L) and arachidonic acid (1 µmol/L; P 〈 0.05).2. The present experiments attempted to elucidate the endothelium dependency of the contraction and to pharmacologically characterize the factors involved in the contraction induced by NA (0.3 µmol/L) in the presence of l-NAME and arachidonic acid in ring preparations of the rat coronary artery.3. The NA (0.3 µmol/L)-induced contraction was attenuated by a chemical remover of the endothelium (saponin at concentrations of 0.1 and 0.4 mg/mL) in a concentration-dependent manner (P 〈 0.05).4. The cyclo-oxygenase (COX)-1 inhibitor flurbiprofen (0.01–1 µmol/L) and the COX-2 inhibitor nimesulide (0.01–1 µmol/L) attenuated the NA-induced contraction in a concentration-dependent manner and the inhibitory effect of flurbiprofen was significantly more potent than that of nimesulide (P 〈 0.05). The 5-lipoxigenase inhibitor ZM-230487 (1 µmol/L) did not affect the NA-induced contraction.5. The thromboxane A2 (TXA2) synthetase inhibitor OKY-046 (30 µmol/L) and the TXA2 antagonist S-1452 (0.1–10 µmol/L) did not attenuate the NA-induced contraction.6. These results indicate that the contraction induced by NA in the rat coronary artery in the presence of l-NAME and arachidonic acid is endothelium dependent and is due to endothelial COX metabolites of arachidonic acid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0305-1870.2005.04242.x
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  • 2
    Electronic Resource
    Electronic Resource
    PARTICIPATION OF VASOPRESSIN IN THE DEVELOPMENT OF CEREBRAL VASOSPASM IN A RAT MODEL OF SUBARACHNOID HAEMORRHAGE (2004)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 31 (2004), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V1 receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5-lipoxygenase inhibitor ZM 230487 on AVP-induced contraction of rat basilar arteries was also investigated.2. After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)-induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats.3. The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059-treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group (P 〈 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin-induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP-induced contraction in the presence of ZM 230487 compared with control (P 〈 0.05).4. The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5-lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2004.03986.x
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  • 3
    Electronic Resource
    Electronic Resource
    Cysteinyl leukotrienes and leukotriene B4 mediate vasoconstriction to arginine vasopressin in rat basilar artery (2005)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Arginine vasopressin (AVP) has been reported to be involved in the development of cerebral vasospasm after haemorrhage and cerebral oedema following ischaemia. Endogenously produced 5-lipoxygenase metabolites are able to contract isolated endothelium-preserved arterial strips and modulate vascular permeability. The present study addresses the role of 5-lipoxygenase and its products, namely cysteinyl leukotrienes (CysLTs) and leukotriene (LT) B4, in the contraction induced by AVP in rat basilar artery.2. Contractile responses to LTD4, LTC4, LTB4 or AVP were assessed in spiral preparations of rat endothelium-intact basilar artery. Contractions to AVP were determined in the absence or presence of 5-lipoxygenase inhibitors or CysLT1 or BLT receptor antagonists. Contractile responses to leukotrienes and AVP are expressed as a percentage of the contraction induced by 80 mmol/L KCl.3. Leukotriene D4, LTC4 and LTB4 acted as vasoconstrictor agents in rat basilar artery, causing contractions (all at concentrations of 1 µmol/L) of 42 ± 13, 54 ± 15 and 25 ± 6% of the response to 80 mmol/L KCl, respectively. A concentration–response curve was constructed for AVP over the range 1 pmol/L to 10 nmol/L and an EC50 value of 0.19 ± 0.02 nmol/L (n = 30) was determinted. The presence of the 5-lipoxygenase inhibitors ZM 230487 (10 nmol/L and 0.1 and 1 µmol/L) and AA 861 (1, 3, 10, and 30 µmol/L), the CysLT1 receptor antagonist MK 571 (3, 10 and 30 µmol/L) or the BLT receptor antagonists CP 105696 and LY 255283 (3, 10 and 30 µmol/L for both) in the organ bath significantly attenuated the contractions induced by AVP in rat basilar artery (P 〈 0.05).4. The experimental results of the present study provide the first evidence for the involvement of CysLTs and LTB4 in the in vitro constriction induced by AVP in rat basilar artery. In the context of previously reported involvement of AVP in the development of cerebral vasospasm and oedema, the present study draws attention to the potential role played by the 5-lipoxygenase pathway in these pathological processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2005.04300.x
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  • 4
    Electronic Resource
    Electronic Resource
    Possible activation of intracellular β-adrenoceptors by extraneuronally accumulated isoprenaline in perfused rat heart (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 531-538 
    Details
    ISSN: 1432-1912
    Keywords: Functionally effective intracellular β-adrenoceptors ; Extraneuronal accumulation ; Chronotropic response to isoprenaline ; Rat heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two rat hearts were perfused in series by a modified Loewi's method. The recipient heart was perfused with the perfusate collected from the donor heart. 1. After perfusion with 3H-isoprenaline in the presence of tropolone, an inhibitor of catechol-O-methyltransferase, the donor heart was washed out with amine-free medium containing tropolone and corticosterone. The heart rate of the recipient heart increased after the change to the perfusate from the donor heart during the wash-out. After wash-out the heart rate of the donor heart (which had accumulated 43.4 pmol. g−1 3H-isoprenaline) was higher than that of the recipient heart (which had accumulated 0.44 pmol · g−1 3H-isoprenaline), and the rates of efflux of 3H-isoprenaline from both hearts were similar. 2. After perfusion with 3H-isoprenaline and corticosterone in the absence of tropolone, the enhanced heart rate of the donor heart decreased during wash-out with amine-free medium in the presence of corticosterone. The heart rate of the recipient heart increased after the medium change to the perfusate from the donor heart, and the heart rates in both hearts were similar after wash-out. Only small amounts of 3H-isoprenaline remained in both hearts after wash-out, and the rates of efflux of 3H-isoprenaline from both hearts were similar. 3. After perfusion with 3H-isoprenaline in the presence of tropolone, the effects of propranolol and atenolol on the heart rate during wash-out with amine-free medium containing tropolone and corticosterone were compared. The inhibitory effect of propranolol on the heart rate was significantly greater than that of atenolol. 4. These findings provide pharmacological evidence for functionally effective intracellular β-adrenoceptors in the rat heart, because the heart with high extraneuronal accumulation of isoprenaline had a higher heart rate than that with low accumulation, although the concentration of isoprenaline in the extracellular space was similar and because a lipophilic β-adrenoceptor blocking agent (propranolol) inhibited the heart rate more effectively than a hydrophilic β-adrenoceptor blocking agent (atenolol) did.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00182727
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 145-148 
    Details
    ISSN: 1432-1912
    Keywords: Perfused rat heart ; 3H-Isoprenaline ; Extraneuronal accumulation ; Antiarrhythmic drugs ; Tetrodotoxin ; β 2-Adrenoceptor antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of class I, II, III and IV antiarrhythmic drugs (as classified by Vaughan Williams 1974), tetrodotoxin and β 2-adrenoceptor antagonists on the extraneuronal accumulation of isoprenaline were examined in isolated rat hearts perfused with 3H-isoprenaline (1 μmol/l) and tropolone (100 μmol/l) for 30 min at a constant flow rate (6.5 ml/min) at 40°C. Quinidine (class I), verapamil (IV), diltiazem (IV), dilazep (IV), nifedipine (IV), tetrodotoxin and butoxamine, at a concentration of 10 μmol/l, significantly decreased the extraneuronal accumulation of isoprenaline. The present study demonstrated that quinidine (class I) and all of the calcium channel blockers (class IV) had potent inhibitory effects on the extraneuronal accumulation of isoprenaline. The concentrations of these drugs needed for this decrease were nearly comparable to those needed to suppress isoprenaline-tropolone-induced ventricular fibrillation (Sone et al. 1985a). The antiarrhythmic effects of quinidine and calcium channel blockers in this experimental model may be partly due to a decrease in the extraneuronal accumulation of isoprenaline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505814
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of extraneuronal uptake inhibitors on the positive chronotropic response to isoprenaline and on the accumulation of isoprenaline in perfused rat heart after inhibition of catechol-O-methyl transferase (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 123-128 
    Details
    ISSN: 1432-1912
    Keywords: Isoprenaline ; Heart rate ; COMT inhibition ; Extraneuronal uptake inhibitor ; Intracellular β-adrenoceptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were carried out in isolated perfused rat hearts. 1. The presence of tropolone (100 \gmol/l), an inhibitor of catechol-O-methyl transferase (COMT), significantly potentiated the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/1). 2. Two uptake2 inhibitors, 3-O-methylisoprenaline (100 gmol/1) and normetanephrine (100 \gmmol/l), induced a positive chronotropic response, but corticosterone (100 \gmmol/l) and hydrocortisone (100 gmol/1) had no such effect. 3. 3-O-methylisoprenaline (100 \gmmol/l) and normetanephrine (100 \gmmol/l) enhanced the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/1). Corticosterone (100 \gmmol/l) potentiated the positive chronotropic response to isoprenaline (0.1 and 1 nmol/1). Hydrocortisone (30 \gmmol/l) enhanced the response to 0.1 nmol/l isoprenaline but did not affect the positive chronotropic responses to 1, 3 or 10 nmol/l isoprenaline. 4. The addition of uptake2 inhibitors (3-O-methylisoprenaline, 100 gmol/1; normetanephrine, 100 \gmmol/l; corticosterone, 100 \gmmol/l) to the perfusion medium significantly reduced the positive chronotropic response to the perfusion with isoprenaline (3 nmol/l) and tropolone (100 \gmmol/l). 5. The accumulation of 3H-isoprenaline in the heart perfused with 3H-isoprenaline (1, 10 and 100 nmol/1) was significantly increased by the presence of tropolone (100 \gmmol/l): the accumulation for 1, 10 and 100 nmol/1 of 3H-isoprenaline was 5.07, 47.0 and 500 pmol/g, respectively. 6. The high accumulation observed during perfusion with 3H-isoprenaline (3 nmol/1) and tropolone (100 gmol/1) was significantly decreased by the addition of an uptake2 inhibitor, 3-O-methylisoprenaline (100 gmol/1), normetanephrine (100 gmol/1) or corticosterone (100 \gmmol/l), but not by hydrocortisone (30 \gmmol/l). 7. From these results, it is suggested that the inhibitory effects of uptake2 inhibitors on the positive chronotropic response to isoprenaline in the presence of a COMT inhibitor might be related to the decrease in accumulation of isoprenaline in the perfused rat hearts, and that the extraneuronally accumulated isoprenaline in the rat heart might activate intracellular \gb-adrenoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177712
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  • 7
    Electronic Resource
    Electronic Resource
    Changes in the incidence and duration of ventricular fibrillation in dependence on the extraneuronal accumulation of isoprenaline in the perfused rat heart (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 76-81 
    Details
    ISSN: 1432-1912
    Keywords: Perfused rat heart ; 3H-Isoprenaline ; Extraneuronal accumulation ; Ventricular fibrillation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between the accumulation of isoprenaline and the incidence and duration of ventricular fibrillation was investigated in the perfused rat heart. Isolated rat hearts were perfused with 3H-isoprenaline (1 μmol/l) for 30 min at a constant flow rate of 6.5 ml/min at a temperature between 40 and 41° C. Electrocardiograms were recorded during the perfusion period and the isoprenaline content of the tissue was measured after the perfusion. The accumulation of isoprenaline was significantly increased and the duration of ventricular fibrillation was significantly prolonged by the presence of tropolone (100 μmol/l). When extraneuronal uptake inhibitors such as normetanephrine (100 μmol/l), 3-O-methylisoprenaline (100 μmol/l) or phenoxybenzamine (1 μmol/l) were added to the perfusion fluid containing 3H-isoprenaline (1 μmol/l) and tropolone (100 μmol/l), the accumulation of isoprenaline was sifnificantly decreased, the incidence of ventricular fibrillation was significantly reduced and the duration of ventricular fibrillation was significantly shortened. There was a significant correlation for dependence of duration of ventricular fibrillation on the isoprenaline content of rat hearts perfused with various extraneuronal uptake inhibitors in the presence of tropolone (correlation coefficient [r]=0.62, P〈0.001). These results indicate that the accumulation of isoprenaline in perfused rat hearts relates to the occurrence and duration of ventricular fibrillation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498854
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