Bimodal action of [Asu^1,7]eel-calcitonin on phosphoinositide hydrolysis in cultured anterior pituitary cells

[Asu^1,7]Eel-calcitonin, a semisynthetic analog of eel-calcitonin disolaying high stability and full biological activity, was used to study the effect of calcitonin on phosphoinositide turnover in cultured anterior pituitary cells. Incubation of cells with [Asu^1,7]eel-calcitonin produced a slight, cocentration-dependent increase in [³H]inositol monophosphate accumulation, without modifying thyrotropin-releasing hormone (TRH)-stimulated phosphoinositide hydrolysis. This effect was correlated with a stimulatory action on prolactin secretion. Conversely, a long-term preincubation with [Asu^1,7]eel-calcitonin reduced basal as well as TRH-induced [³H]inositol monophosphate formation. This effect was concentration-dependent, was not due to an increase of cyclic AMP intracellular levels, and was attenuated in the presence of maximally effective concentrations of TRH. Such a long incubation in the presence of [Asu^1,7]eel-calcitonin resulted in a marked inhibition of prolactin secretion. The present data confirm and extend previous findings showing an interference of calcitonin with the intracellular cascade consequent to membrane phospholipase C activation and further support a role for calcitonin in the modulation of hormome secretion at the pituitary.