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  • 1
    Electronic Resource
    Electronic Resource
    α1B- but not α1A-adrenoceptors mediate inositol phosphate generation (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 341 (1990), S. 385-387 
    Details
    ISSN: 1432-1912
    Keywords: α-Adrenoceptors ; α1A-Adrenoceptors ; α1B-Adrenoceptors ; Second messenger ; Inositol phosphates
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We used novel highly subtype-selective antagonists to study whether α1A- and/or α1B-adrenoceptors mediate the stimulation of inositol phosphate generation by noradrenaline in rat cerebral cortex. Phentolamine (10 μM) and prazosin (100 nM) completely abolished the stimulated inositol phosphate generation. The α1A-selective antagonists 5-methyl-urapidil (100 nM) and (+)− and (−)-niguldipine (10 nM) caused only weak inhibition or none at all although these concentrations occupied α1A-adrenoceptors almost completely. In contrast, pretreatment with the irreversible α1B-selective chloroethylclonidine reduced the noradrenaline-stimulated inositol phosphate generation by 76 ± 8%. These data demonstrate that α1B-adrenoceptors couple to inositol phosphate generation; the signal transduction system of α1A-adrenoceptors remains unclear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180666
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of α1A- and α1B-adrenoceptor coupling to inositol phosphate formation in rat kidney (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 592-598 
    Details
    ISSN: 1432-1912
    Keywords: α1A-adrenoceptors ; α1B-adrenoceptors ; Rat kidney ; Inositol phosphates ; G protein ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have compared the coupling mechanisms of rat renal α1A- and α1B-like adrenoceptors to inositol phosphate formation. The experiments were performed in parallel in native renal tissue preparations and in those where α1B-adrenoceptors had been inactivated by treatment with 10 μmol/l chloroethylclonidine for 30 min at 37°C; renal slices were used in most experiments but isolated renal cells were also used in some cases. The Ca2+ chelating agent, EGTA (5 mmol/l), reduced noradrenaline-stimulated inositol phosphate formation in native but enhanced it in chloroethylclonidine-treated renal slices. The inhibitory effect of EGTA was not mimicked by 100 nmol/l nifedipine. Inactivation of 87% of cellular Gi by 16–20 h treatment with 500 ng/ml pertussis toxin did not significantly affect noradrenaline-stimulated inositol phosphate formation in isolated renal cells but abolished the inhibitory effect of chloroethylclonidine. The adenylate cyclase activator, forskolin (20 μmol/l), inhibited noradrenaline-stimulated inositol phosphate formation in native and chloroethylclonidine-treated slices, and the inhibitory effects of chloroethylclonidine treatment and forskolin were additive. We conclude that in rat kidney inositol phosphate formation via α1B-like adrenoceptors may involve the influx of extracellular Ca2+ and a pertussis toxin-sensitive G-protein but is insensitive to inhibition by forskolin. In contrast α1A-like adrenoceptor-mediated inositol phosphate formation does not require the presence of extracellular Ca2+ or of Gi and is sensitive to inhibition by forskolin. In comparison to published data from other model systems we further conclude that the signaling mechanisms of α1-adrenoceptor subtypes may depend on their cellular environment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169362
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Endothelin-induced inositol phosphate formation in rat kidney. Studies on receptor subtypes, G-proteins and regulation during ontogenesis (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 572-578 
    Details
    ISSN: 1432-1912
    Keywords: Endothelin-receptors ; Kidney ; Inositol phosphates ; G-protein ; Ontogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to characterize the properties of endothelin (ET)-receptor subtypes mediating inositol phosphate (IP)-formation in rat kidney and their regulation during ontogenesis. In renal cortical slices of adult rats (12–16 weeks old) ET's concentration-dependently increased IP-formation with an order of potency ET -1 ≫ ET 3. While the non-selective ET receptor antagonist bosentan (10 μM) completely suppressed ET-induced IP-formation, the ETA-receptor antagonist BQ-123 (10 μM) inhibited it only by 70%, the ETB-receptor antagonist IRL 1038 (1 μM) by 25%; combined application of BQ-123 + IRL 1038 caused complete inhibition of ET-1-induced IP-formation. Pretreatment of isolated renal cells with pertussis toxin (PTX, 500 ng/ml) overnight did not attenuate but significantly increased ET-1-induced IP-formation. Ontogenetic studies in renal slices from neonatal, 1, 2, 3, 6, 12 and 24 weeks old rats revealed that ET-1-induced IP-formation maturation-dependently declined being highest in neonatal rats (increase: 169% over basal) and lowest in 24 weeks old rats (increase: 47% over basal). This decline in ET-induced IP-formation was accompanied by a decrease in renal ET receptor number and the amount of immunodetectable Gq/11 (assessed by Western-blotting using the QL-antiserum). Moreover, ET receptor subtypes changed during the maturation process: from neonates to 12 weeks old rats number and functional responsiveness of ETA-receptors declined, while that of ETB-receptors increased. We conclude that in adult rat renal cortex ET-induced IP-formation is mediated by activation of both ETA- and ETB-receptors and does not involve a PTX-sensitive G-protein. ET-induced IP-formation declines during the maturation process; this is associated with a decrease in ET-receptor number and the immunodetectable amount of Gq/11.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170830
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    α1A and α1B-adrenoceptors enhance inositol phosphate generation in rat renal cortex (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 180-185 
    Details
    ISSN: 1432-1912
    Keywords: α1-Adrenoceptor ; Inositol phosphates ; Rat kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the role of α1A and α1B-adrenoceptors in noradrenaline- and methoxamine-stimulated inositol phosphate accumulation in rat renal cortical slices. [3H]Prazosin binding studies with and without inactivation of α1B-adrenoceptors by chloroethylclonidine treatment suggested that noradrenaline lacks relevant selectivity for α1-adrenoceptor subtypes. Both agonists stimulated [3H]inositol phosphate accumulation with similar maximal effects. The α1A-selective antagonists 5-methyl-urapidil and (+)-niguldipine inhibited inositol phosphate formation by both agonists with shallow biphasic curves but the high affinity component was only 15%–31% and 38%–41%, respectively. The irreversible α1B-selective antagonist chloroethylclonidine inhibited inositol phosphate generation by both agonists by 54%–57%. In contrast to our previous data in rat cerebral cortical slices; we conclude that in rat renal cortex both α1A- and α1B-adrenoceptors are involved in noradrenaline-and methoxamine-stimulated inositol phosphate generation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169264
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    NPY and carbachol raise Ca2+ in SK-N-MC cells by three different mechanisms (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 370-374 
    Details
    ISSN: 1432-1912
    Keywords: NPY receptor ; Muscarinic acetylcholine receptor ; Ca2+ ; Inositol phosphates
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have compared the mechanism of NPY-and carbachol-stimulated Ca2+ increases in SK-N-MC cells. NPY stimulated Ca2+ mobilization via a pertussis toxin-sensitive mechanism. Carbachol stimulated Ca2+ mobilization and influx via pertussis toxin-insensitive and -sensitive mechanisms, respectively. Carbachol but not NPY stimulated inositol phosphate accumulation by a pertussis toxin-insensitive mechanism. We conclude that carbachol promotes Ca2+ influx via a pertussis toxin-sensitive G protein and Ca2+ mobilization via a pertussis toxin-insensitive G-protein coupling to inositol phosphate generation; NPY stimulates Ca2+ mobilization via a pertussis toxin-sensitive G protein without apparent involvement of inositol phosphates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00176612
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    Paper (German National Licenses)
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