Minenko A, Oehme P
Institute of Drug Research, Academy of Sciences of the GDR, Berlin.
Biomed Biochim Acta. 1987;46(6):461-7.
The effect of SP (1.10(-6) M) on the 32P incorporation into inositol phospholipids from rat adrenal medulla slices has been examined. After 20 s, a decreased 32P incorporation into all inositol phospholipids was found (most expressed for phosphatidyl-inositol-4,5-bisphosphate) without changes in phosphatidylcholine/phospatidylserine fraction. During 5 min exposure to SP the 32P incorporation into phosphatidylinositol-4,5-bisphosphate returned up to the control level, whereas that into phosphatidylcholine/phosphatidylserine fraction strongly decreased. A within-one-sample comparison of the radioactivity of each phospholipid against that in the phosphatidylcholine/phosphatidylserine fraction reveals a "phosphatidylinositol effect". A possible regulation mechanism of catecholamine secretion by SP in relation to changes in inositol phospholipids is discussed.
研究了速激肽（1.10(-6) M）对大鼠肾上腺髓质切片中32P掺入肌醇磷脂的影响。20秒后，发现所有肌醇磷脂中的32P掺入量均减少（磷脂酰肌醇-4,5-二磷酸最为明显），而磷脂酰胆碱/磷脂酰丝氨酸组分无变化。在暴露于速激肽5分钟的过程中，磷脂酰肌醇-4,5-二磷酸中的32P掺入量恢复至对照水平，而磷脂酰胆碱/磷脂酰丝氨酸组分中的32P掺入量则大幅下降。对每种磷脂的放射性与磷脂酰胆碱/磷脂酰丝氨酸组分中的放射性进行样本内比较，揭示了一种“磷脂酰肌醇效应”。讨论了速激肽通过肌醇磷脂变化对儿茶酚胺分泌的可能调节机制。
