Prevention by 7-oxo-prostacyclin of the calcium paradox in rat heart: Role of the sarcolemmal (Na,K)-ATPase
✍ Scribed by Attila Ziegelhöffer; Tatiana Ravingerová; Andrej Džurba; Narcisa Tribulová; Jan Slezák; Albert Breier; László Szekeres
- Publisher
- Springer
- Year
- 1996
- Tongue
- English
- Weight
- 711 KB
- Volume
- 160-161
- Category
- Article
- ISSN
- 0300-8177
No coin nor oath required. For personal study only.
✦ Synopsis
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 Ca(2+)-paradox in the rat heart. Pretreatment of the animals with 7-oxo-prostacyclin (PGI2) 24-48 h prior to the experiment prevented fairly the Ca(2+)-depletion-induced depression in (Na,K)ATPase activity and the accompanying structural and functional damage to the heart and sarcolemma during Ca(2+)-depletion as well as the development of Ca(2+)-paradox during the subsequent Ca(2+)-repletion. Pretreatment with PGI2 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 Ca(2+)-deprivation, the capability of heart sarcolemma to maintain sodium extrusion remains preserved, the expected aggravation of Ca(2+)-overload injury to Ca(2+)-paradox that would develop during Ca(2+)-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.