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Platelet-activating factor induced a negative inotropic effect in isolated rat cardiomyocytes, inhibiting systolic [Ca2+]i increase by up to 52% and cell shortening by up to 50%.
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Platelet-activating factor induces a negative inotropic effect in rat cardiomyocytes by decreasing systolic intracellular calcium concentration.
We investigated the effects of platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) on intracellular Ca2+ concentration ([Ca2+]i) and cell length in isolated and field-stimulated rat cardiomyocytes. [Ca2+]i and cell length of field-stimulated cells were determined simultaneously by confocal laser scan microscopy by using the fluorescent Ca2+ dye Fluo-3. PAF (10(-12)-10(-8) M) inhibited systolic [Ca2+]i increase in a time- and concentration-dependent manner. Maximal effects were observed after an incubation time of 6-8 min, resulting in a 17% (10(-12) M), 41% (10(-10) M), and 52% (10(-8) M PAF) inhibition of systolic [Ca2+]i increase. A time- and concentration-dependent decrease in simultaneously measured cell shortening also was demonstrated. Cell shortening was inhibited by 10% (10(-12) M), 32% (10(-10) M), and 50% (10(-8) M) after an incubation time of 8 min. The effects of PAF could be antagonized by the PAF-receptor antagonist WEB 2170. These data demonstrate that PAF receptor-dependently induces a negative inotropic effect, which is correlated with a decrease in systolic [Ca2+]i and is most likely not due to a decrease in myofilament sensitivity.
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Pietsch et al. (1998) studied this question. Platelet-activating factor (PAF) was evaluated on Systolic [Ca2+]i increase and cell shortening. Platelet-activating factor induced a negative inotropic effect in isolated rat cardiomyocytes, inhibiting systolic [Ca2+]i increase by up to 52% and cell shortening by up to 50%.
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