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  • 1
    Electronic Resource
    Electronic Resource
    Role of inhibitory G protein α-subunits in adenylyl cyclase desensitization
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 82 (1991), S. C215-C221 
    Details
    ISSN: 0303-7207
    Keywords: Adenylyl cyclase ; Desensitization ; G-protein ; Up-regulation ; βγ-Dimers
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0303-7207(91)90022-K
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of metabolites between mitochondria and cytosol of cultured fibroblastoid rat heart cells
    Amsterdam : Elsevier
    FEBS Letters 100 (1979), S. 125-128 
    Details
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(79)81146-1
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  • 3
    Electronic Resource
    Electronic Resource
    Multiple forms of the sodium pump with different affinities for digitalis
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 18 (1986), S. 25 
    Details
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/S0022-2828(86)80106-7
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of vanadate in cultured rat heart muscle cells. Vanadate transport, intracellular binding and vanadate-induced changes in beating and in active cation flux
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 597 (1980), S. 364-383 
    Details
    ISSN: 0005-2736
    Keywords: (Heart muscle cell) ; Cation flux ; Rb^+ uptake ; Vanadate
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2736(80)90113-3
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  • 5
    Electronic Resource
    Electronic Resource
    Stimulatory (insulin-mimetic) and inhibitory (ouabain-like) action of vanadate on potassium uptake and cellular sodium and potassium in heart cells in culture
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 687 (1982), S. 79-93 
    Details
    ISSN: 0005-2736
    Keywords: (Heart cell) ; Insulin ; K^+ uptake ; Na^+ uptake ; Ouabain ; Vanadate
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2736(82)90172-9
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  • 6
    Electronic Resource
    Electronic Resource
    Chronic muscarinic cholinoceptor stimulation increases adenylyl cyclase responsiveness in rat cardiomyocytes by a decrease in the level of inhibitory G-protein α-subunits (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 27-34 
    Details
    ISSN: 1432-1912
    Keywords: Muscarinic cholinoceptor ; Adenylyl cyclase Gi-protein ; \ Adrenoceptor ; Heart cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Exposure of neonatal rat cardiomyocytes for 3 days to the muscarinic cholinoceptor agonist carbachol led to a concentration-dependent increase in adenylyl cyclase stimulation by the \-adrenoceptor agonist isoproterenol by up to 115% (at 1 mmol/l carbachol). In addition, direct adenylyl cyclase stimulation by forskolin was increased in carbachol (1 mmol/l)-treated cells by 32010. Pretreatment of the rat cardiomyocytes with pertussis toxin, which enhances adenylyl cyclase activity by a functional inactivation of the inhibitory G-protein (Gi), was performed to investigate the possible role of Gi proteins in carbachol-induced sensitization of adenylyl cyclase stimulation. After pretreatment of the cells with pertussis toxin, the carbachol-mediated increase in forskolin-stimulated adenylyl cyclase activity was lost and the carbachol-mediated increase in \-adrenoceptor-stimulated adenylyl cyclase activity was attenuated. Labelling of the 40 kDa pertussis toxin substrates in cardiomyocyte membranes was decreased by carbachol in a concentration-dependent manner by up to 34010 (at 1 mmol/l carbachol). The number and affinity of \1-adrenoceptors was unaltered following the chronic carbachol treatment. The specific protein synthesis inhibitor Pseudomonas exotoxin A was used to study whether the carbachol-induced decrease in the level of pertussis toxin-sensitive G-proteins and increase in adenylyl cyclase activity depend on de-novo protein synthesis. Pseudomonas exotoxin A inhibits peptide chain elongation by ADP-ribosylating elongation factor 2. Treatment of the cells with 1 ng/ml Pseudomonas exotoxin A for 3 days led to a reduction in the subsequent ADP-ribosylation of elongation factor 2 in the cytosol of the heart muscle cells by 57%. Exposure of the cells to 1 mmol/l carbachol for 3 days increased ADP-ribosylation of elongation factor 2 by 40% concomitant with a slight (about 20%) increase in the total protein content of the cardiomyocytes. The partial protein synthesis inhibition by Pseudomonas exotoxin A had no influence on the carbachol-induced decrease in the level of pertussis toxin-sensitive G-proteins. Similarly, the carbachol-induced increase in adenylyl cyclase responsiveness also remained unaltered by Pseudomonas exotoxin A. The data presented indicate that chronic muscarinic cholinoceptor agonist treatment decreases the level of α-subunits of Gi- proteins. This decrease in Giα- subunits is apparently at least in part responsible for the observed increase in adenylyl cyclase responsiveness after chronic carbachol treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169060
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  • 7
    Electronic Resource
    Electronic Resource
    Successful closure of a traumatic pulmonary arteriovenous fistula of the main pulmonary artery (1982)
    Springer
    World journal of surgery 6 (1982), S. 484-488 
    Details
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le cas d'un homme de 53 ans qui avait présenté une plaie pénétrante de la poitrine lors de la deuxième guerre mondiale est rapporté. Trente quatre ans plus tard une fistule artérioveineuse pulmonaire consécutive à cette blessure fut découverte et traitée par simple suture. La revue de la littérature montre que ce cas représente la cinquième observation de fistule artério-veineuse post-traumatique et le premier cas de succès obtenu sans résection pulmonaire, par simple suture.
    Notes: Abstract The case of a 53-year-old man who suffered from a penetrating chest injury in World War II is reported. Thirty-four years later, an arteriovenous pulmonary fistula arising from this injury was diagnosed and closed by direct suture. A review of the literature indicates that this is the fifth case of a pulmonary fistula of traumatic origin, and the first case in which such a fistula has been successfully closed without resection of lung tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01657687
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  • 8
    Electronic Resource
    Electronic Resource
    Chronic muscarinic cholinoceptor stimulation increases adenylyl cyclase responsiveness in rat cardiomyocytes by a decrease in the level of inhibitory G-protein α-subunits (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1994), S. 27-34 
    Details
    ISSN: 1432-1912
    Keywords: Key words Muscarinic cholinoceptor ; Adenylyl cyclase Gi-protein ; β-Adrenoceptor ; Heart cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Exposure of neonatal rat cardiomyocytes for 3 days to the muscarinic cholinoceptor agonist carbachol led to a concentration-dependent increase in adenylyl cyclase stimulation by the β-adrenoceptor agonist isoproterenol by up to 115% (at 1 mmol/l carbachol). In addition, direct adenylyl cyclase stimulation by forskolin was increased in carbachol (1 mmol/l)-treated cells by 32%. Pretreatment of the rat cardiomyocytes with pertussis toxin, which enhances adenylyl cyclase activity by a functional inactivation of the inhibitory G-protein (Gi), was performed to investigate the possible role of Gi-proteins in carbachol-induced sensitization of adenylyl cyclase stimulation. After pretreatment of the cells with pertussis toxin, the carbachol-mediated increase in forskolin-stimulated adenylyl cyclase activity was lost and the carbachol-mediated increase in β-adrenoceptor-stimulated adenylyl cyclase activity was attenuated. Labelling of the 40 kDa pertussis toxin substrates in cardiomyocyte membranes was decreased by carbachol in a concentration-dependent manner by up to 34% (at 1 mmol/l carbachol). The number and affinity of β 1-adrenoceptors was unaltered following the chronic carbachol treatment. The specific protein synthesis inhibitor Pseudomonas exotoxin A was used to study whether the carbachol-induced decrease in the level of pertussis toxin-sensitive G-proteins and increase in adenylyl cyclase activity depend on de-novo protein synthesis. Pseudomonas exotoxin A inhibits peptide chain elongation by ADP-ribosylating elongation factor 2. Treatment of the cells with 1 ng/ml Pseudomonas exotoxin A for 3 days led to a reduction in the subsequent ADP-ribosylation of elongation factor 2 in the cytosol of the heart muscle cells by 57%. Exposure of the cells to 1 mmol/l carbachol for 3 days increased ADP-ribosylation of elongation factor 2 by 40% concomitant with a slight (about 20%) increase in the total protein content of the cardiomyocytes. The partial protein synthesis inhibition by Pseudomonas exotoxin A had no influence on the carbachol-induced decrease in the level of pertussis toxin-sensitive G-proteins. Similarly, the carbachol-induced increase in adenylyl cyclase responsiveness also remained unaltered by Pseudomonas exotoxin A. The data presented indicate that chronic muscarinic cholinoceptor agonist treatment decreases the level of α-subunits of Gi-proteins. This decrease in Gia-subunits is apparently at least in part responsible for the observed increase in adenylyl cyclase responsiveness after chronic carbachol treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169060
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Influence of digitalis and diuretics on ouabain binding sites on human erythrocytes (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 87-92 
    Details
    ISSN: 1432-1440
    Keywords: Ouabain binding ; Erythrocytes ; Diuretics ; Digitalis effect ; Receptor kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been reported that during chronic treatment with digitalis, the number of digitalis binding sites is increased in human erythrocytes [22]. From this finding a tachyphylaxis for cardiac glycosides has been postulated. We reinvestigated this problem in several groups of patients. The number of3H-ouabain binding sites per erythrocyte in control persons (group I) was 214±60,n=43 (x±SD). The dissociation constant (KD) was 1.8±0.5 nM. Thirteen patients (group II) taking cardiac glycosides only, for at least 6 months, had 281±99 (p〈0.05) ouabain binding sites per single red cell, KD=1.8±0.7 nM. Group III (34 patients) took digitalis for more than 6 months and diuretics for at least 3 months (352±126 (p〈0.001), KD=1.6±0.6). Twenty-three of these (group IV) were taking a combination with “K+-saving” diuretics (336±194 (p〈0.01), KD=1.6±0.5) and (group V, 11 patients) a combination with “K+-losing” diuretics (462±133 (p〈0.001), KD=1.4±0.4). Nine patients (group VI) had a chronic hypokalemia, mainly due to taking furosemide (437±98 (p〈0.001), KD=1.5±0.4). Four control persons took 50 mg hydrochlorothiazide daily for more than 4 months without measurable K+-losses and without changes in ouabain binding sites. It is concluded from these findings that diuretic treatment with chronic hypokalemia in addition to digitalis is accompanied by a significant increase in ouabain binding sites in human red cells. Although the difference between control persons and those taking cardiac glycosides only, is statistically significant (p〈0.05), the biological relevance is questionable because of considerable overlap of the values. Receptor affinity was unchanged under all circumstances. A change in the number of ouabain binding sites — if occurring also in the heart — may go along with an altered digitalis sensitivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01769668
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  • 10
    Electronic Resource
    Electronic Resource
    Cardiac glycoside tolerance in cultured chicken heart muscle cells — A dose-dependent phenomenon (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 1253-1264 
    Details
    ISSN: 1432-1440
    Keywords: Cardiac glycosides ; Tolerance ; Heart cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In cultured heart muscle cells from 10–13 day-old chicken embryos, the effects of acute (4 h) and chronic (3 days) exposure of the cells to varying concentrations of ouabain have been studied. In these cells, the cardiac glycoside ouabain binds to a specific cardiac glycoside receptor (KD=4 × 10−7 M; 750,000 receptors/cell). Binding to this receptor results in inhibition of active Na+/K+-transport [EC50 for active (86Rb+ + K+)-influx=4 × 10−6 M], and in an increase in beating velocity (“positive inotropic effect”;; EC50=4 × 10−7 M); toxic signs (arrhythmias) appear at concentrations ≥ 6 × 10−7 M. During exposure of the cells to 3 × 10−6 M ouabain for 3 days, tolerance develops with respect to both the positive inotropic and the toxic effect. The mechanism underlying this tolerance is identified as an increase in the number of active sodium pump molecules per cell, while the binding properties of the cardiac glycoside receptor remain unchanged. The development of cardiac glycoside tolerance is only observed in the presence of severe impairment of Na+/K+-homeostasis, due to cardiac glycoside-induced inhibition of active Na+/K+-transport. This, however, only occurs in the presence of toxic (receptor occupation ≥ 60%), but not in the presence of positive inotropic, non-toxic (receptor occupation 20–60%), ouabain concentrations. We conclude that the development of cardiac glycoside tolerance during long-term treatment in patients with heart failure should not occur with submaximal dose regimens, when toxic signs (arrhythmias) are absent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01738450
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