Bromocriptine restores angiotensin II response in pituitary hyperplasia

In estrogen-induced pituitary hyperplasia AII-evoked prolactin release is d ecreased and the octapeptide does not generate a spike elevation in [Ca2+]( i) in vitro. We studied whether or not bromocriptine could restore AII resp onse in diethylstilbestrol treated rats. Go-administration of bromocriptine resulted in involution of pituitary size and lowering of serum prolactin. In vitro, prolactin release per cell was reduced in the hyperplastic group, and levels were not significantly increased by in vivo bromocriptine treat ment. Immunocytochemical analysis revealed that hyperplastic pituitaries co ntained fewer prolactin granules than control pituitaries, and that bromocr iptine, did not increase prolactin storage. Nevertheless, in this group, pr olactin response to AII increased, and AII evoked a consistent spike in [Ca 2+](i), albeit lower than in the control group. Such spike was abolished by thapsigargin, and not by removal of extracellular calcium or by K+, indica ting that it was mainly dependent on intracellular calcium stores, as in no rmal cells. We conclude that bromocriptine treatment partially restores AII response in the hyperplastic pituitary. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.