The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Abstract

The direct effects of α-and β-adrenergic agents on PRL and β-endorphin (β-END) secretion in vitro by porcine pituitary cells have been investigated. Pituitary glands were obtained from mature gilts, which were ovariectomised (OVX) one month before slaughter. Ovariectomised gilts, assigned to four groups, were primed with: (1) vehicle (OVX); (2) and (3) oestradiol benzoate (EB; 2.5 mg/100 kg b.w.) at 30-36 h (OVX+EB I) and 60-66 h (OVX+EB II) before slaughter, respectively; and (4) progesterone (P 4 ; 120 mg/100 kg b.w.) for 5 consecutive days before slaughter (OVX+P 4 ). Isolated anterior pituitary cells were submitted to 3.5 h incubation in the presence of GnRH, α-and β-adrenergic agonists [phenylephrine (PHEN) and isoproterenol (ISOP), respectively], or α-and β-adrenergic blockers [phentolamine (PHENT) and propranolol (PROP), respectively]. The culture media were assayed for PRL (exp. I) and β-endorphin-like immunoreactivity (β-END-LI) (experiment II). In experiment I, GnRH did not influence PRL release by pituitary cells in all experimental groups. Some of tested doses of adrenergic agonists, PHEN and ISOP, increased PRL release from pituitary cells of OVX gilts, but not from those of OVX+EB I animals. In the OVX+EB II group, PHEN alone, but ISOP with PROP, potentiated PRL secretion by the cells. In OVX+P 4 animals, PHEN alone or in combination with PHENT and also ISOP alone or with PROP enhanced PRL output from the cells. In experiment II, addition of GnRH increased β-END-LI release from pituitary cells only in the OVX+EB II group. PHEN and PHENT potentiated β-END-LI secretion by pituitary cells in OVX+EB II and OVX+P 4 groups, while ISOP and PROP increased β-END-LI secretion by the cells of OVX and OVX+EB II animals. In turn, in the OVX+EB I group, effect of PHENT and PROP on PRL secretion by pituitary cells was inhibitory. In conclusion, our results suggest that adrenergic agents can modulate PRL and β-END secretion by porcine pituitary cells in a manner dependent on the hormonal status of gilts.

The effects of <i>mu</i>-, <i>delta</i>- and <i>kappa</i>-opioid receptor activation on <i>in vitro</i> prolactin secretion by anterior pituitary cells of cyclic gilts

“…during the estrogen-induced LH surge) or following treatment with progesterone, but did not influence the hormone secretion by the cells derived from untreated OVX gilts (Bogacka et al, 2002). Adrenergic agents (acting through α-and β-receptors) also appeared to affect prolactin secretion in vitro by pituitary cells of gilts, treated and untreated with steroids (Siawrys et al, 2003). In addition, the differentiated modulation of prolactin secretion by pituitary cells in vitro following treatment with agonists of opioid receptors was described herein for pigs at various stages of the oestrous cycle.…”

Differential involvement of cAMP/PKA-, PLC/PKC- and Ca2+/calmodulin-dependent pathways in GnRH-induced prolactin secretion and gene expression in grass carp pituitary cells

“…The in vitro studies for PRL regulation via pituitary action of GnRH, however, are not consistent and vary with sex, reproductive stages and neonatal development. For examples, PRL secretion induced by GnRH was demonstrated in pituitary fragments/pituitary cells prepared from human ( 64 ), sheep ( 43 ) and neonatal rat ( 65 ) but not in other species (e.g., in porcine pituitary cells) ( 44 , 45 ). Of note, the PRL-releasing effect of GnRH was observed in pituitary cells prepared from female sheep during the breeding season but not in other time of the year ( 43 ).…”

“…Apparently, PRL induction by GnRH may serve as a signal input from the hypothalamo-pituitary axis to trigger the reproductive functions of PRL. Although PRL regulation by GnRH has also been reported in mammals, the information is restricted to PRL release and the results obtained are not consistent, as stimulatory ( 41 – 43 ) and no effect have been documented ( 44 , 45 ). For stimulatory action, GnRH-induced PRL secretion could be associated with the elevation of IP 3 ( 46 ) and cAMP levels ( 47 , 48 ) or indirect action via local signals produced by gonadotrophs ( 49 , 50 ).…”