Role of calcium in dopaminergic regulation of TRH- and angiotensin II-stimulated prolactin release

Abstract

The contributions of intracellular and extracellular calcium to thyrotropin-releasing hormone (TRH)- and angiotensin II (ANG II)-stimulated prolactin (PRL) release and the role of calcium in dopaminergic inhibition of these events were examined because of unresolved controversies in these areas. Dispersed normal female rat anterior pituitary cells were used to evaluate radiocalcium fluxes and the intracellular calcium concentration ([Ca]i). Both peptides increased PRL release, fractional 45Ca2+ efflux, and [Ca]i in a spike and plateau pattern, and neither increased 45Ca2+ uptake. In a low-calcium buffer, TRH and ANG II stimulated less than 5% of the normal PRL response, yet efflux was at least 50% of normal and [Ca]i was 20-40% of normal. Dopamine reduced TRH-stimulated PRL release by greater than 90% and abolished the plateau, yet the calcium responses to TRH were at least 50% of normal. Although dopamine prevented the plateau component of peptide-stimulated [Ca]i, the plateau phase of efflux persisted. Thus TRH and ANG II may control at least two cell-associated calcium pools, one readily depleted and the other highly resistant to depletion, without evidence for stimulation of calcium uptake. Dopamine inhibits PRL release stimulated by these peptides, with a relatively greater influence on the plateau component, through mechanisms only minimally related to calcium flux. Dopamine may slightly increase the extrusion of calcium mobilized by these peptides and thus may limit the anticipated increase in [Ca]i.