Journal
CELL CALCIUM
Volume 29, Issue 2, Pages 73-83Publisher
ELSEVIER SCI LTD
DOI: 10.1054/ceca.2000.0158
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To investigate how mechanical stress is sensed by cardiomyocytes and translated to cardiac hypertrophy, cardiomyocytes were subjected to stretch while measuring phospholipase C (PLC) and phospholipase D (PLD) activities and levels of intracellular calcium ions ([Ca2+](i)) and pH. In stretched cardiomyocytes, PLC activity increased 2-fold after 30 min, whereas PLD activity hardly increased at all. Mechanical stress induced by prodding or by cell stretch increased [Ca2+](i) by a factor 5.2 and 4, respectively. Gadolinium chloride (stretch-activated channel blocker) attenuated the prodding-induced and stretch-induced [Ca2+](i) rise by about 50%. Blockade of ryanodine receptors by a combination of Ruthenium Red and procaine reduced the [Ca2+](i) rise only partially. Diltiazem (L-type Ca2+ channel antagonist) blocked the prodding-induced [Ca2+](i) rise completely, and reduced the stretch-induced [Ca2+](i) rise by about 50%. The stretch-induced [Ca2+](i) rise was unaffected by U73122, an inhibitor of PLC activity. Stretch did not cause cellular alkalinization. In conclusion, in cardiomyocytes, PLC and [Ca2+](i) levels are involved in the stretch-induced signal transduction, whereas PLD plays apparently no role. The stretch-induced rise in [Ca2+](i) in cardiomyocytes is most probably caused by Ca2+ influx through L-type Ca2+ channels and stretch-activated channels, leading to Ca2+-induced Ca2+-release from the SR via the ryanodine receptor. (C) 2001 Harcourt Publishers Ltd.
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