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  • Electronic Resource  (4)
  • Cyclic AMP  (2)
  • β-Receptors  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 275 (1972), S. 95-104 
    ISSN: 1432-1912
    Keywords: Temperature ; β-Receptors ; Guinea-Pig Atrium ; Affinity ; Adrenergic Drugs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using electrically stimulated guinea-pig atria the influence of temperature on the contractility and on the efficacy of some β-sympathomimetic and-lytic drugs, was studied. The following results were obtained. 1. Raising the temperature of the bath fluid from 25–42°C decreased significantly the developed amplitude of contraction under control conditions, whereas dT/dt max values were not altered. The maximal developed tension induced by the sympathomimetic drugs decreased at 42°C. The corresponding dT/dt max values, on the other hand, were increased by elevation of the temperature. 2. The dose-response curves of the sympathomimetic drugs isoprenaline (IPN), Th 1165a and orciprenaline (OPN) were shifted to the right when the temperature was increased from 25–42°C. The affinity of IPN at 33°C was found about 30- and 100-times higher than that of Th 1165a and OPN, respectively. 3. The β-adrenolytic drug pindolol (LB 46), as well as the cardioselective β-blocker, practolol, antagonized the β-sympathomimetic effects evoked by IPN and Th 1165a in a competitive manner. As indicated by the pA2 values, pindolol had a 100-times higher affinity than practolol. The present results lead to the conclusion that, on the guinea-pig atrium, the agonist β-receptor reaction depends on the metabolic rate of this organ.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 275 (1972), S. 105-113 
    ISSN: 1432-1912
    Keywords: Sympathomimetic Affinity ; β-Receptors ; Temperature ; Metabolic State ; Isolated Organs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments on isolated organs-rabbit ileum, guinea-pig trachea and atrium — with different “β-receptor subtypes” were carried out in order to determine whether changes of the metabolic state or of the extracellular pH were able to alter the responsiveness of these receptors to sympathomimetic amines. 1. Guinea-Pig Atrium. Lowering of the pH of the bath fluid from 7.48 to 6.79 resulted in a significant decrease of the affinity of isoprenaline (IPN) calculated as the pD2-value. Metabolic inhibition induced by iodoacetic acid (IAA) (5×10−5 M) increased the affinity of Th 1165a. 2. Rabbit Ileum. The affinity of IPN was not changed by lowering the pH, even to values of 6.11. At this pH the spontaneous motility was already markedly impaired. IAA (2.4×10−5 M) caused a moderate increase in the affinity of IPN whereas those of Th 1165a and orciprenaline (OPN) were elevated 10-fold. 3. Guinea-Pig Trachea. Lowering of the pH caused a decrease of the pD2-values of IPN and in particular of Th 1165a. The metabolic inhibitor IAA had no influence upon the pD2 value of IPN. 4. The present results favour the existence of only one type of β-receptor which changes its sensitivity depending on the metabolic state. It seems therefore very likely that the affinity of sympathomimetic drugs depends not only on the structure of the β-receptor but also on the metabolic state of the tissue.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 67 (1989), S. 799-803 
    ISSN: 1432-1440
    Keywords: Cystic Fibrosis ; Blood cells ; Beta-adrenoceptors ; Cyclic AMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several in vivo and in vitro studies have suggested that children suffering from cystic fibrosis (CF) might have a general defect of beta-adrenoceptors on the cell surface which might account for an unbalanced secretory process. In order to investigate if this view holds true, we determined the beta-adrenoceptor density and affinity on lymphocytes by means of radioligand studies using 125-iodo-cyano-pindolol (125-ICYP) in 20 children with CF. Cyclic AMP (cAMP) response was also investigated after specific beta-adrenoceptor stimulation with isoprenaline (IPN) and after direct stimulation of the adenylate cyclase with forskolin in lymphocytes. Children with CF and controls have identical numbers and affinities of beta-adrenoceptors on lymphocytes. The cyclic AMP response was identical in CF- and in age-matched control children regardless whether adenylate cyclase was stimulated directly or via beta-adrenoceptors. In conclusion, the data support the view that no general adrenoceptor or adenylate cyclase defect exists in CF. As several studies have found abnormal reactions to adrenergic stimuli in CF patients, we presume that there is a defect beyond the level of adrenergic receptors and cAMP which remains to be identified.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 134 (1980), S. 45-50 
    ISSN: 1432-1076
    Keywords: Exercise induced asthma (EIA) ; Catecholamines ; Cyclic AMP ; a-Adrenergic blockade ; Allergic asthma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to provoke exercise induced asthma (EIA) a test which involved running for 7 min was performed with 21 asthmatic children. Eleven children not only developed a highly significant increase in airway resistance (Rt), but showed also a 4-fold increase in plasma noradrenaline (NA) levels. In 10 children who did not develop EIA only a 1.5-fold increase of NA could be observed. Following exercise cyclic AMP showed an identical increase in both groups studied, whereas adrenaline levels remained uninfluenced. Tests carried out after administration of phentolamine by inhalation showed a significant inhibition of post-exercise bronchoconstriction. It is concluded that EIA originates from a-receptor stimulation which is mediated by excessive noradrenaline release. However, since disodium cromoglycate—which does not act via adrenergic mechanisms—also protected against EIA, other factors should be involved. In 5 children with allergic asthma, asthmatic attacks were accompanied by a significant decrease in cAMP, whereas noradrenaline levels remained uninfluenced. Thus, evidence appears that both types of asthma result from different autonomic dysfunctions.
    Type of Medium: Electronic Resource
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