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  • mitochondrial contraction  (2)
  • swelling and contraction of heart mitochondria  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Respiration-dependent contraction of swollen heart mitochondria: Participation of the K+/H+ antiporter (1988)
    Springer
    Journal of bioenergetics and biomembranes 20 (1988), S. 229-242 
    Details
    ISSN: 1573-6881
    Keywords: K+/H+ antiport ; mitochondria ; mitochondrial contraction ; dicyclohexylcarbodiimide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Respiration-dependent contraction of heart mitochondria swollen passively in K+ nitrate is activated by the ionophore A23187 and inhibited by Mg2+. Ion extrusion and osmotic contraction under these conditions are strongly inhibited by quinine, a known inhibitor of the mitochondrial K+/H+ antiporter, as measured in other systems. The inhibition by quinine is relieved by the exogenous antiporter nigericin. Respiration-dependent contraction is also inhibited by dicyclohexylcarbodiimide (DCCD) when reacted under conditions known to inhibit K+/H+ antiport (Martinet al., J. Biol. Chem. 259, 2062–2065, 1984). These studies strongly support the concept that K+ is extruded from the matrix by the endogenous K+/H+ antiporter and that inhibition of this component by quinine or DCCD inhibits respiration-dependent contraction. The extrusion of K+ nitrate is accompanied by a respiration-dependent efflux of a considerable portion of the endogenous Mg2+. This Mg2+ efflux does not occur in the presence of nigericin or when the mitochondrial Na+/H+ antiporter is active. Mg2+ efflux may take place on the K+/H+ antiporter. DCCD, reacted under conditions that do not result in inhibition of the K+/H+ antiporter, blocks a monovalent cation uniport pathway. This uniport contributes to futile cation cycling at elevated pH, and its inhibition by DCCD stimulates respiration-dependent contraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00768396
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of quinine on K+ transport in heart mitochondria (1984)
    Springer
    Journal of bioenergetics and biomembranes 16 (1984), S. 379-390 
    Details
    ISSN: 1573-6881
    Keywords: Quinine ; quinacrine ; mitochondrial K+/H+ antiport ; swelling and contraction of heart mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem. 257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00743233
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    K+/H+ antiport in mitochondria (1988)
    Springer
    Journal of bioenergetics and biomembranes 20 (1988), S. 193-209 
    Details
    ISSN: 1573-6881
    Keywords: Mitochondria ; K+/H+ antiport ; mitochondrial swelling ; mitochondrial contraction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Mitochondria contain a latent K+/H+ antiporter that is activated by Mg2+-depletion and shows optimal activity in alkaline, hypotonic suspending media. This K+/H+ antiport activity appears responsible for a respiration-dependent extrusion of endogenous K+, for passive swelling in K+ acetate and other media, for a passive exchange of matrix42K+ against external K+, Na+, or Li+, and for the respiration-dependent ion extrusion and osmotic contraction of mitochondria swollen passively in K+ nitrate. K+/H+ antiport is inhibited by quinine and by dicyclohexylcarbodiimide when this reagent is reacted with Mg2+-depleted mitochondria. There is good suggestive evidence that the K+/H+ antiport may serve as the endogenous K+-extruding device of the mitochondrion. There is also considerable experimental support for the concept that the K+/H+ antiport is regulated to prevent futile influx-efflux cycling of K+. However, it is not yet clear whether such regulation depends on matrix free Mg2+, on membrane conformational changes, or other as yet unknown factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00768394
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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