Abstract
The depolarisation‐induced influx of 45Ca2+ into anterior pituitary tissue and GH3 cells through ‘L’‐type, nimodipine‐sensitive channels was investigated. In anterior pituitary prisms, phorbol esters, activators of protein kinase C, caused an enhancement of K+‐induced 45Ca2+ influx. However, in the GH3 anterior pituitary cell line, phorbol esters inhibited K+‐induced 45Ca2+ influx. The modulation by phorbol esters in both tissues was stereo‐specific and time‐ and concentration‐dependent. The diacylglycerol analogue, 1,2‐dioctanoyl sn‐glycerol was able to mimic the phorbol ester‐induced enhancement of calcium influx into anterior pituitary pieces, but was ineffective in GH3 cell. 1,2‐Diactanoyl sn‐glycerol may selectively activate an isoform of protein kinase C which is responsible for enhanced ‘L’‐type Ca2+‐channel activity.