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  • 1
    Electronic Resource
    Electronic Resource
    Depolarisation of guinea-pig visceral smooth muscle causes hydrolysis of inositol phospholipids (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 78-82 
    Details
    ISSN: 1432-1912
    Keywords: Smooth muscle ; Phosphoinositides ; Inositol lipids ; Depolarisation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Increasing concentrations of KCl caused a progressive stimulation of contractile activity in guinea-pig jejunal longitudinal smooth muscle strips, accompanied by increased production of [3H]inositol phosphates in smooth muscle fragments pre-labelled with myo-[3H]inositol. The concentration-response curve for contractility lay to the left of that for [3H]inositol phosphate production. Both responses showed a dependency on the presence of Ca2+ in the incubation medium. K+-induced contractility was abolished by D600 or by Mn2+, whereas stimulated [3H]inositol phosphate formation persisted in the presence of these Ca2+-channel blockers. The simultaneous addition of high KCl concentrations together with a maximal concentration of neurotransmitter (carbamylcholine or substance P) produced additive stimulation of [3H]inositol phosphate production. Enhanced production of [3H]inositol phosphates was also observed under a variety of conditions known to cause smooth muscle depolarisation, including omission from the incubation medium of Na+ or K+, and in response to ouabain or veratridine. The results suggest that inositol lipid hydrolysis in visceral longitudinal smooth muscle may be triggered by depolarisation, an event which causes the entry of Ca2+ into the cell but which is not generally believed to cause the release of stored Ca2+ within the cell. However, calcium entry seems not to be essential for the effect on inositol lipid hydrolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569664
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Regulatory volume increase in rat pancreatic β-cells (1997)
    Springer
    Pflügers Archiv 435 (1997), S. 227-230 
    Details
    ISSN: 1432-2013
    Keywords: Key words Pancreas ; Islet cells ; Cell volume ; Na+-2Cl ; -K+ cotransporter ; Na+-H+ exchange ; Cl ; -HCO3 ; exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This study investigated regulatory volume increase (RVI) in rat pancreatic β-cells. Volume changes in isolated β-cells were measured by a video-imaging method. Cell shrinkage was induced by exposure to solutions made hypertonic by the addition of 100 mM mannitol. In HEPES-buffered solutions, β-cells exhibited an RVI which was almost completely abolished by 10 μM bumetanide. These data indicate that Na+-2Cl–-K+ cotransporters make a major contribution to RVI in β-cells. In HCO3 –-buffered solutions, however, an RVI was observed in the presence of 10 μM bumetanide. This bumetanide-insensitive component of RVI was inhibited by 100 μM amiloride or 100 μM 4,4’-diisothiocyanatostilbene-2,2’-disulphonic acid (DIDS). These data suggest that, in addition to the Na+-2Cl–-K+ cotransporter, functionally coupled Na+-H+ exchangers and Cl–-HCO3 – exchangers may also contribute to RVI in pancreatic β-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050505
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    Paper (German National Licenses)
    Fulltext
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