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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