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  • 1
    Electronic Resource
    Electronic Resource
    Presence of two Ca2+ influx components in internal Ca2+-pool-depleted rat parotid acinar cells (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 105-111 
    Details
    ISSN: 1432-2013
    Keywords: Key words Ca2+ entry ; Kinetics ; Thapsigargin ; Parotid cells ; Fura-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The molecular mechanism(s) involved in mediating Ca2+ entry into rat parotid acinar and other non-excitable cells is not known. In this study we have examined the kinetics of Ca2+ entry in fura-2-loaded parotid acinar cells, which were treated with thapsigargin to deplete internal Ca2+ pools (Ca2+-pool-depleted cells). The rate of Ca2+ entry was determined by measuring the initial increase in free cytosolic [Ca2+] ([Ca2+]i) in Ca2+-pool-depleted, and control (untreated), cells upon addition of various [Ca2+] to the medium. In untreated cells, a low-affinity component was detected with K Ca = 3.4 ± 0.7 mM (where K Ca denotes affinity for Ca2+) and V max = 9.8 ± 0.4 nM [Ca2+]i /s. In thapsigargin-treated cells, two Ca2+ influx components were detected with K Ca values of 152 ±  79 μM (V max = 5.1 ± 1.9 nM [Ca2+]i/s) and 2.4 ±  0.9 mM (V max = 37.6 ± 13.6 nM [Ca2+]i/s), respectively. We have also examined the effect of Ca2+ and depolarization on these two putative Ca2+ influx components. When cells were treated with thapsigargin in a Ca2+-free medium, Ca2+ influx was higher than into cells treated in a Ca2+-containing medium and, while there was a 46% increase in the V max of the low-affinity component (no change in K Ca), the high-affinity component was not clearly detected. In depolarized Ca2+-pool-depleted cells (with 50 mM KCl in the medium) the high-affinity component was considerably decreased while there was an apparent increase in the K Ca of the low-affinity component, without any change in the V max. These results demonstrate that Ca2+ influx into parotid acinar cells (1) is increased (four- to five-fold) upon internal Ca2+ pool depletion, and (2) is mediated via at least two components, with low and high affinities for Ca2+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050111
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  • 2
    Electronic Resource
    Electronic Resource
    Role for protein kinase in Ca2+-dependent feedback modulation of divalent cation influx in internal-Ca2+-store-depleted rat parotid gland cells (1997)
    Springer
    Pflügers Archiv 433 (1997), S. 464-471 
    Details
    ISSN: 1432-2013
    Keywords: Key words Ca2+ entry ; Mn2+ entry ; Protein kinase ; Staurosporine ; K-252a ; Salivary glands
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Divalent cation (Ca2+ and Mn2+) influx, stimulated by internal Ca2+ store depletion, into rat parotid acinar cells is inhibited by conditions which increase protein phosphorylation [T. Sakai and I.S. Ambudkar (1996) Am J Physiol 271:C284–C294]. The present study examines the involvement of this protein phosphorylation and Ca2+ in the store-dependent inactivation of divalent cation entry. Internal Ca2+ store depletion, achieved by incubation (30 min) of cells in nominally Ca2+-free medium containing either carbachol or thapsigargin, stimulated Ca2+, and Mn2+, influx into cells. In either case, inclusion of 1.5 mM Ca2+ for the last 5 min of incubation resulted in a decrease in Ca2+ (33–41%) and Mn2+ (50%) influx, which could not be accounted for by internal Ca2+ store refill. The inhibition was prevented when internal-store-depleted cells were treated (prior to incubation with Ca2+) with either staurosporine or K-252a, but not with H-7 or KN-93. Refilling of internal Ca2+ store(s) in carbachol-treated cells (incubation with Ca2++atropine) induced complete inhibition of divalent cation influx, which was not prevented by treatment with protein kinase inhibitors. These data suggest the staurosporine-sensitive (and K-252a-sensitive) protein phosphorylation is not involved in Ca2+-store-refilling-dependent inactivation of Ca2+ influx but mediates a Ca2+-dependent feedback modulation of divalent cation influx in rat parotid gland acinar cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050301
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  • 3
    Electronic Resource
    Electronic Resource
    Measurement of airway resistance in anesthetized and paralyzed subjects: proposal for evaluation of K1 values (1988)
    Springer
    Journal of anesthesia 2 (1988), S. 139-145 
    Details
    ISSN: 1438-8359
    Keywords: Airway resistance ; Measurement ; General anesthesia ; airflow ; Lung volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of lung volume and respiratory airflow on airway resistance were studied in five anesthetized and paralyzed patients. Airway resistance measured during the inspiratory phase with intermittent constant airflow inflatoins decreased in inverse correlationship to increases in lung volume. Airway resistance measured during the expiratory phase with an airway interruption technique, on the other hand, increased with a linear relationship to the expiratory airflow as expressed by a function of Y = K1 + K2X. K1, calculated from the values of airway resistance corresponding to three different airflows, was unaffected by intentional expiratory resistance loading. Thus, simultaneously with the measurement of airway resistance by this method, expiratory gas sampling with a Douglas bag can be done if necessary. Since the K2 value of the endotracheal tube used in this study (Portex® I.D. 8 mm, length 26 cm) was quite high (5.0 cmH2O·1−2·sec2), depending on the airflow, the presence of the endotracheal tube strongly affected the measurement of airway resistance during general anesthesia. K1 measured by the above method, however, may be considered as the best way to evaluate the lower airway resistance independent of either lung volume or expiratory airflow. (Sakai T, Yoshida H, Yano H et al.: Measurement of airway resistance in anesthetized and paralyzed subjects: proposal for evaluation of K1 values. J Anesth 2: 139–145, 1988)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054080020139
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Parathyroid hormone stimulates phosphoinositide metabolism and intracellular calcium mobilization in osteoblast-like clone MC3T3-E1 cells (1991)
    Springer
    Journal of bone and mineral metabolism 9 (1991), S. 19-25 
    Details
    ISSN: 1435-5604
    Keywords: Osteoblast ; Parathyroid Hormone ; Ins(1,4,5)P3 ; Cytosolic Ca2+ ; 1,2 Diacylglycerol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of parathyroid hormone (rat 1–34 fragment, rPTH) on phosphoinositide metabolism and intracellular Ca2+ mobilization were studied in a osteoblast-like clone MC3T3-E1 cells. rPTH caused a transient rise in intracellular Ca2+ in a dose-dependent manner. Significant Ca2+ increase was still observed under the extracellular Ca2+-free condition. In addition, 100nM rPTH stimulated rapid formation of both 1,2-diacylglycerol (1,2-DAG) and inositol 1,4,5-trisphosphate (Ins(1,4,5)P3), indicating agonist-triggered hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2). The current observations suggested that the rPTH-induced increase of intracellular Ca2+ was in part due to internal Ca2+ release mediated by Ins(1,4,5)P3. These results indicate possible involvement of phosphoiniositide metabolism in signal transduction of PTH-stimulated osteoblastic cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02374930
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    Paper (German National Licenses)
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