Different pathways of endothelin/sarafotoxin-stimulated phosphoinositide hydrolysis in myocytes.

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.