Superfusion of rat anterior pituitary cell aggregates with 10-min pulses of 0.1–10 nM angiotensin II (AII) resulted in a prompt and concentration-dependent rise of PRLrelease. The effect could be blocked by saralasin, an AII receptor antagonist. The response to AII, but not that to TRH, was rapidly desensitized:a 10 nM AII pulse caused an 80% depression of the response to a subsequent 10 nM pulse given 50 min later. The data provide a possible functional significance for the renin-angiotensin system recently demonstrated in the anterior pituitary.

The dynamics of dopamine (DA) action on PRL release was studied in superfused rat anterior pituitary cell aggregates, cultured for for 5 days either in conventional or in serum-free defined medium. In aggregates cultured in conventional medium 0.1-1 nM DA applied for 20 min provoked a rapid and concentration-dependent inhibition of PRL release, lasting only a few minutes, after which there was a gradual rise in secretion up to near baseline levels. A sustained inhibition was obtained from DA concentrations more than or equal to 10 nM. When DA, used at the latter concentration, was withdrawn from the superfusion medium, a marked rebound secretion of PRL occurred, exceeding basal release for as long as 40-50 min. Rebound secretion was not followed by a compensatory fall in secretion rate. After a 10-min pulse of 10 or 30 nM DA, the amount of PRL released above baseline was considerably higher than the amount of PRL not released during the time DA was present. The latter stimulation of PRL release was not seen after a 40- or 90-min exposure time to DA. However, when DA was given for 40 min in 10 pulses of 4 min (4 min DA on 4 min DA off), a clear-cut stimulation of PRL release followed the termination of the pulses. When the serum used in the culture medium was extracted with dextran-coated charcoal, post-DA rebound secretion of PRL was markedly diminished. The latter secretion pattern partially reappeared when the extracted serum was supplemented with 10 nM dexamethasone. DA had similar effects on PRL release in aggregates cultured in serum-free defined medium. Dexamethasone did not affect DA-inhibition but strongly stimulated post-DA rebound, and this effect was potentiated by T3 present in the defined medium. There was three to four times more PRL secreted in excess of basal release than was inhibited during exposure to DA. The present data suggest a dual action of DA on PRL release: inhibition during tonic exposure to the catecholamine and inhibition-mediated stimulation after pulsatile exposure.

In superfused rat anterior pituitary cell reaggregates, cultured for 5 days in serum-free defined medium, vasoactive intestinal peptide (VIP) concentration-dependently stimulated prolactin (Prl) release but had only a marginal effect on growth hormone (GH) release. When reaggregates were cultured in the presence of 80 nM dexamethasone (Dex) VIP strongly stimulated GH release from a concentration as low as 0.1 nM VIP did not stimulate LH release. Peptide PHI also stimulated GH release but thyrotropin-releasing hormone (TRH) or angiotensin II did not. In fact, TRH slightly but transiently inhibited basal GH release and strongly inhibited VIP-stimulated GH release. GH-releasing factor (GRF) stimulated GH more potently and with higher intrinsic activity than VIP but GRF did not increase Prl release. The present data indicate that under defined hormonal conditions VIP and PHI are capable of stimulating GH release and that TRH can antagonize this effect by a direct action on the pituitary.

The effect of the β-adrenergic agonist isoproterenol (ISO) on c-AMP accumulation and on growth hormone (GH) and prolactin (PRL) release was studied in primary cultures of anterior pituitary cell populations with different proportional number of somatotrophs and lactotrophs, obtained by velocity sedimentation at unit gravity. ISO stimulated c-AMP levels in highly-enriched lactotroph (∼7O%) as well as in highly-enriched somatotroph (∼65%) populations. ISO-stimulated c-AMP accumulation was attenuated by dopamine (DA) in highly enriched lactotroph but not somatotroph populations. In a small-cell population consisting of a much lower proportional number of lactotrophs and somatotrophs, the proportional increase of c-AMP accumulation was several times higher than in the other populations and the effect was not suppressible by DA. In this small-cell population, GH but not PRL release was more responsive to ISO than in the other populations. The present observations are consistent with the interpretation that the changes in c-AMP levels induced by ISO originate in part in somatotrophs and lactotrophs. However, the present data also demonstrate that the most responsive cell population in terms of c-AMP accumulation consists of small cells. The majority of these cells could not be identified. The possibility that these cells may be nonsecreting folliculostellate cells is discussed.

No abstract

No abstract

In superfused anterior pituitary cell aggregates, prolactin release is stimulated by angiotensin II (All) in a concentration-dependent fashion between 0.1 and 10 nM When studied in aggregates prepared from pituitary cell populations separated according to size by unit gravity sedimentation, the PRL response to All was weak in a population enriched in lactotrophs but deprived of gonadotrophs. In other separated populations, the response increased with the proportional number of gonadotrophs. The response also increased when lactotrophs were co-aggregated with an enriched population of gonadotrophs. It is proposed that the PRL response to All is augmented by an intercellular messenger system presumably operating between gonadotrophs and lactotrophs.

No abstract