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  • Articles  (2)
  • cyclic nucleotide hydrolysis  (1)
  • subsarcolemmal Na/Ca ratio  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Prevention by 7-oxo-prostacyclin of the calcium paradox in rat heart: Role of the sarcolemmal (Na,K)-ATPase (1996)
    Springer
    Molecular and cellular biochemistry 160-161 (1996), S. 257-263 
    Details
    ISSN: 1573-4919
    Keywords: 7-oxo-prostacyclin ; calcium paradox ; sarcolemmal (Na,K)-ATPase ; subsarcolemmal sodium ; subsarcolemmal Na/Ca ratio ; calcium overload of the heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract It is demonstrated a fast and significant depression in the sarcolemmal (Na,K)-ATPase activity that occurs as early as 25 sec after the onset of Ca2+ depletion, and participates in the development of Ca2+-paradox in the rat heart. Pretreatment of the animals with 7-oxo-prostacyclin (PG12) 24–48 h prior to the experiment prevented fairly the Ca2+-depletion-induced depression in (Na,K)ATPase activity and the accompanying structural and functional damage to the heart and sarcolemma during Ca2+-depletion as well as the development of Ca2+-paradox during the subsequent Ca2+-repletion. Pretreatment with PGI, was chosen intentionally because previous experiments revealed, that in its late effect the drug is acting via stabilizing the membranes due induction of high activity of (Na,K)-ATPase that has increased affinity to ATP. From results obtained the following may be concluded: If during the phase of Ca2+-deprivation, the capability of heart sarcolemma to maintain sodium extrusion remains preserved, the expected aggravation of Ca2+-overload injury to Ca2+-paradox that would develop during Ca2+-repletion, may be definitely prevented. Sufficiently preserved (Na,K)-ATPase activity, hand in hand with stabilized sarcolemmal structure, may prevent an accumulation of sodium beneath the sarcolemma and consequently also an overexcessive entry of Ca2+ into the myocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00240057
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  • 2
    Electronic Resource
    Electronic Resource
    Long lasting anti-adrenergic effect of 7-oxo-prostacyclin in the heart: a cycloheximide sensitive increase of phosphodiesterase isoform I and IV activities (1994)
    Springer
    Molecular and cellular biochemistry 132 (1994), S. 57-67 
    Details
    ISSN: 1573-4919
    Keywords: heart protection ; 7-oxo-prostacyclin ; cyclic nucleotide hydrolysis ; phosphodiesterase isoenzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Evidence is accumulating that 7-oxo-prostacyclin (7-oxo-PGI2) induces a delayed indirect anti-adrenergic and cytoprotective effect on the myocardium, the mechanism of which is still unclear. To demonstrate that a single application of 7-oxo-PGI2 (50 μg/kg i.m.) 48 h prior to starting experiments attenuates the isoprenaline inducible inotropic response and accumulation of cAMP, isolated hearts of pretreated animals were perfused in the Langendorff mode with and without isoprenaline (1 to 100 nM). The late anti-adrenergic effect of the drug was manifested by a significant attenuation in the elevation of cAMP levels as well as in contractile force development. This effect was not due to changes in cAMP generation as there were identical β1-adrenoceptor densities and affinities (as calculated from [3H]-CGP binding studies), Gi and Gαs protein patterns (as taken from Western blots) as well as adenylyl cyclase activity measurements in the hearts studied. The anti-adrenergic potency of 7-oxo-PGI2, however, was found to be related to a significant rise in cyclic nucleotide hydrolysis by phosphodiesterase (PDE). Using the fast-performance liquid chromatographic separation for PDE isoforms, a significant increase in the activity of PDE isoforms I and IV (260±28 vs 110±12 pmol cGMP/min x enzyme fraction and 77±11 vs 34±3 pmol cAMP/min x enzyme fraction, respectively) was found in the solubilized fraction of cardiac membranes in comparison to untreated controls; PDE IV activity was also increased in the cytosolic fraction (106±14 vs 65±6 pmol cAMP/min x enzyme fraction). The hypothesis that the delayed anti-adrenergic effect of 7-oxo-PGI2 is initiated by an induction and accelerated synthesis of PDE I and IV in the heart is underlined by the fact that cycloheximide suppresses completely both the rise in PDE activities and the anti-adrenergic effects studied. It is suggested that an inducible predominance of cAMP degradation over its generation may be of relevance in processes related to heart protection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925675
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    Paper (German National Licenses)
    Fulltext
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