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Increasing Intracellular Calcium of Guinea Pig Ventricular Myocytes Induced by Platelet Activating Factor through IP 3 Pathway
Author(s) -
Chu WenFeng,
Sun HongLi,
Dong DeLi,
Qiao GuoFen,
Yang BaoFeng
Publication year - 2006
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2006.pto_313.x
Subject(s) - ryanodine receptor , intracellular , extracellular , platelet activating factor , chemistry , calcium , stimulation , medicine , myocyte , endocrinology , calcium in biology , platelet , fura 2 , cytosol , biology , biochemistry , enzyme
We used Fluo‐3/AM to examine the effect of platelet‐activating factor on the intracellular Ca 2+ ([Ca 2+ ] i ) levels in isolated myocytes of guinea pig ventricle. Myocytes were isolated with Langendorff perfusion technique and were challenged with platelet‐activating factor. Addition of platelet‐activating factor (1 pM to 10 nM) significantly increased the [Ca 2+ ] i in the presence and absence of extracellular Ca 2+ . The notion that increases in intracellular Ca 2+ induced by platelet‐activating factor is the result of stimulation of intracellular Ca 2+ pool rather than increasing Ca 2+ influx was further supported by the whole cell patch‐clamp experiments in which the platelet‐activating factor did not alter the activity of L‐type of Ca 2+ channels ( I Ca‐L ). Treatment of myocytes with ryanodine failed to abolish the stimulatory effect of platelet‐activating factor on [Ca 2+ ] i . In contrast, inhibition of IP 3 ‐sensitive Ca 2+ release pool with 2‐aminoethoxydiphenyl borate (2‐APB) blocked the effect of platelet‐activating factor. We conclude that the platelet‐activating factor‐induced increase in intracellular Ca 2+ is mediated by stimulation of IP 3 receptor but not by stimulation of I Ca‐L and ryanodine‐sensitive receptor.