Galron R, Kloog Y, Bdolah A, Sokolovsky M
Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Israel.
Eur J Pharmacol. 1990 Jan 23;188(1):85-8. doi: 10.1016/0922-4106(90)90251-r.
Aging of rat heart myocytes in culture is accompanied by approximately 50% reduction in endothelin (ET)/sarafotoxin (SRTX) receptor-binding capacity as well as in the induction of phosphoinositide (PI) hydrolysis. Treatment of aged cultures under conditions yielding myocytes with a lipid composition similar to that in young cultures restored all the ET/SRTX receptors; at the same time it re-established only the endothelin-induced but not the sarafotoxin-induced PI-hydrolysis response. Thus more than one mechanism may stimulate PI metabolism.
培养的大鼠心肌细胞老化伴随着内皮素（ET）/蛙皮毒素（SRTX）受体结合能力以及磷酸肌醇（PI）水解诱导作用降低约50%。在能使心肌细胞脂质组成与年轻培养物中相似的条件下处理老化培养物，可使所有ET/SRTX受体恢复；同时，它仅重新建立了内皮素诱导的而非蛙皮毒素诱导的PI水解反应。因此，可能有不止一种机制刺激PI代谢。
