Speziale N, Speziale E H, Pasquini J M
Biochim Biophys Acta. 1985 Aug 22;836(1):14-8. doi: 10.1016/0005-2760(85)90214-0.
Rat renal medullary slices prelabeled with [14C]arachidonic acid generate [14C]diacylglycerol within 1 min of exposure to bradykinin action. Production of [14C]diacylglycerol is transient. 2 min after the addition of bradykinin, the levels of metabolite reach the maximum, but decrease thereafter. Simultaneously, bradykinin induces a parallel decrease of the radioactivity in phosphatidylinositol. No degradation of other phospholipids is observed, and triacylglycerol is not affected. The degradation of [14C]phosphatidylinositol to [14C]diacylglycerol indicated the presence of phospholipase C activity. Preincubation of prelabeled slices with 2 mM dibutyryl cyclic AMP prevents both the generation of diacylglycerol and the degradation of phosphatidylinositol. Neither mepacrine nor indomethacin block diacylglycerol production and phosphatidylinositol breakdown. We conclude that, when rat renal medullary slices are stimulated with bradykinin, phosphatidylinositol-specific phospholipase C is activated.
预先用[14C]花生四烯酸标记的大鼠肾髓质切片在暴露于缓激肽作用1分钟内产生[14C]二酰基甘油。[14C]二酰基甘油的产生是短暂的。加入缓激肽2分钟后，代谢物水平达到最大值，但随后下降。同时，缓激肽导致磷脂酰肌醇中的放射性平行下降。未观察到其他磷脂的降解，三酰甘油也未受影响。[14C]磷脂酰肌醇降解为[14C]二酰基甘油表明存在磷脂酶C活性。用2 mM二丁酰环磷酸腺苷对预先标记的切片进行预孵育可防止二酰基甘油的生成和磷脂酰肌醇的降解。米帕林和吲哚美辛均不阻断二酰基甘油的产生和磷脂酰肌醇的分解。我们得出结论，当用缓激肽刺激大鼠肾髓质切片时，磷脂酰肌醇特异性磷脂酶C被激活。
