title: Extracellulary administered lysophosphatidylcholine causes Ca2+ efflux from freshly isolated adult rat cardiomyocytes.
abstract: It has previously been reported that ischemia and reperfusion of the heart cause accumulation of lysophosphatidylcholine (LPC) within the myocardium. While it is known that LPC causes the transient increase of intracellular free Ca2+ concentration ([Ca2+]i) during contraction of cardiac cells, little is known about the mechanism for decreasing [Ca2+]i in cardiomyocytes during LPC accumulation. Since cumulative elevation in [Ca2+]i leads to irreversible injury to cardiomyocytes, elevated [Ca2+]i must be restored to an unstimulated level to maintain cell functions. In the present study, we therefore examined the effect of LPC on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. LPC stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-7)M-10(-5)M). Other lysophospholipids, which are generated from phospholipids of the cell membrane, failed to induce 45Ca2+ efflux from the cells. Dilazep and K-7259, which are known to inhibit the increase in [Ca2+]i caused by LPC, likewise reduced 45Ca2+ efflux caused by LPC addition. Furthermore, the LPC-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. On the other hand, inhibitors of Na+/Ca2+ exchange, amiloride and 5-(N,N-dimethyl)-amiloride, inhibited LPC induced 45Ca2+ efflux. These results suggest that LPC stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange on the plasma membrane of the cells.
authors.affiliation: Department of Cardiovascular Surgery, School of Medicine, University of Tokushima, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Itoh
authors.forename: M
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: T
authors.initials: T
authors.lastname: Kitagawa
authors.forename: Y
authors.initials: Y
authors.lastname: Fukuta
authors.forename: T
authors.initials: T
authors.lastname: Hori
authors.forename: H
authors.initials: H
authors.lastname: Houchi
authors.forename: T
authors.initials: T
authors.lastname: Tamaki
authors.forename: I
authors.initials: I
authors.lastname: Katoh
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D008244:Lysophosphatidylcholines / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D008244:Lysophosphatidylcholines; D019831:Sodium-Calcium Exchanger; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; C039465:5-dimethylamiloride; D000584:Amiloride; D000255:Adenosine Triphosphate; D012964:Sodium; D002118:Calcium