Griffiths E J, Brunt R V
Department of Biochemistry, University of Bath, UK.
J Mol Cell Cardiol. 1990 Mar;22(3):303-10. doi: 10.1016/0022-2828(90)91463-h.
Isolated rat hearts were perfused with various external Ca2+ concentrations and with various Ca2+ uptake antagonists. Compared to control activities (at 1.2 mM Ca2+), 0.6 mM Ca2+ and Ca2+ antagonists inhibited triglyceride lipase (TGL) and stimulated glycerol 3-phosphate acyltransferase (GPAT). Raising external Ca2+ concentration above the control value had no effect on TGL activity but GPAT activity was greatly reduced. Therefore, it appears that GPAT, but not TGL, will respond to increases in [Ca2+]. During ischaemia the activity of TGL is increased and that of GPAT is inhibited by beta-adrenergic activation. On reperfusion, TGL activity returns to pre-ischaemic values but GPAT activity is further reduced. In this study pre-perfusion of hearts with the Ca2+ antagonist diltiazem (10(-6) M) produced the following effects on enzyme activity during ischaemia and reperfusion: after 10 min ischaemia, TGL activity was increased and GPAT activity decreased to the same extent as seen during ischaemia in control hearts; however, on reperfusion of diltiazem-perfused hearts, the activities of both TGL and GPAT returned to pre-ischaemic values. These results suggest that Ca2+ entry on reperfusion is responsible for the reperfusion-induced decrease in GPAT activity.
将离体大鼠心脏用不同的细胞外钙离子浓度和不同的钙离子摄取拮抗剂进行灌注。与对照活性（在1.2 mM钙离子浓度下）相比，0.6 mM钙离子和钙离子拮抗剂抑制了甘油三酯脂肪酶（TGL）并刺激了3-磷酸甘油酰基转移酶（GPAT）。将细胞外钙离子浓度提高到对照值以上对TGL活性没有影响，但GPAT活性大大降低。因此，似乎GPAT而非TGL会对[Ca2+]的增加做出反应。在缺血期间，TGL的活性增加，而GPAT的活性被β-肾上腺素能激活所抑制。再灌注时，TGL活性恢复到缺血前的值，但GPAT活性进一步降低。在本研究中，用钙离子拮抗剂地尔硫䓬（10(-6) M）对心脏进行预灌注，在缺血和再灌注期间对酶活性产生了以下影响：缺血10分钟后，TGL活性增加，GPAT活性降低，与对照心脏缺血期间的情况相同；然而，在对用地尔硫䓬灌注的心脏进行再灌注时，TGL和GPAT的活性都恢复到缺血前的值。这些结果表明，再灌注时钙离子的进入是再灌注诱导的GPAT活性降低的原因。
