Relationship between ACTH Secretion and Corticoid Binding to Specific Receptors in Perifused Adenohypophyses

Self Cite

Alterations in the ionic composition of the medium and different secretagogues have been used in order to study the mechanism of release of ACTH from superfused neurointermediate lobes (NIL) of rat hypophysis. We showed that: (a) a tenfold increase of K in the medium caused a reversible and repeatable stimulation of the ACTH release; (b) removal of Ca ‘ ^: reversibly abolished the stimulating effect of high K⁺: (c) removal of Ca’ had no effect on the stimulating effect of a hypothalaniic extract (HE); (d) in the latter case, a reversible significant weakening was obtained by the addition of EDTA in the Ca⁺⁺-free medium; (e) dbc-AMP caused a reversible and repeatable stimulation of the ACTH release; (f) comparable results were obtained for anterior lobes (AL) superfused in the same conditions. From these data we can conclude that Ca⁺⁺ is necessary for the stimulation of the hormonal release and that factors such as K or dbc-AMP can mimic the in vitro stimulating effect of a HE. Similarities, which appear in this study, between the modulation of the ACTH release from NIL and AL. led us to support the idea that, in vivo, a release of ACTH from the NIL, may occur in physiological conditions.

Section: Discussionsupporting

confidence: 91%

<i>In vitro</i> Regulation of ACTH Release from Neurointermediate Lobe of Rat Hypophysis

Briaud¹,

Koch²,

Lutz-Bucher³

et al. 1980

Self Cite

“…Cells were extracted by sonication and the extract centrifuged at 10,000 g for 10 min. ACTH and cAMP were measured by specific radioimmunoassays, as previously reported [3,11 ].…”

Section: Incubation Proceduresmentioning

confidence: 99%

The Vasopressin Receptor System in the Neonatal Pituitary Gland: Evidence for Reduced Binding Capacity and Signal Transmission

Koch¹,

Lutz-Bucher²

1990

The present study was aimed at evaluating the capacity of anterior pituitary cells from neonatal rats to bind arginine vasopressin (AVP) and show AVP-receptor-mediated signal transmission. We found that in cultures of pituitary cells of 10-day-old pups, in contrast to cultures of cells of adults, AVP was unable to trigger sustained adrenocorticotropin (ACTH) secretion and, in addition, was also less potent in synergizing with the effect of corticotropin-releasing factor (CRF) on both ACTH output and cyclic AMP formation. Binding studies revealed the existence of a much lower number of AVP receptor sites in membranes of neonatal pituitary gland than in those of adult tissue (32.3 ± 9.0 and 137.6 ± 6.2 fmol/mg protein, respectively), although the binding of agonists and the apparent molecular weight (M_r about 120,000) of the receptors were similar. Activation by phorbol ester PMA of protein kinase C, a messenger involved in AVP action, resulted in a dose-related enhancement of ACTH secretion that was 2–3 times smaller for immature corticotrophs than for mature ones. Importantly, PMA treatment allowed AVP to significantly stimulate ACTH secretion from neonatal cells, while it failed to similarly affect AVP-evoked hormone output from adult tissue. Our results indicate that pituitary corticotrophs of rat pups fail to properly transduce AVP-receptor-mediated signalling and, thereby, suggest an explanation for the postnatal ‘stress nonresponsive period’.

“…Neurointermediate pitui taries were dissected out and pools of 5 -10 glands placed in KrebRinger bicarbonate buffer supplemented with 0.2% glucose and 0.1% bovine serum albumin (pH 7.4). They were transferred into perifusion chambers and perifused as already described [6]. The flow rates of buffer was 0.2 ml/min, and 5-min period fractions were collected in tubes containing 0.1 ml of I M HCI.…”

mentioning

confidence: 99%

Modulation by Leu-Enkephalin of Peptide Release from Perifused Neurointermediate Pituitary

Zein¹,

Lutz-Bucher²,

Koch³

1984

This study examines the effect of leu-enkephalin on K⁺, veratridine and isoproterenol stimulation of vasopressin (AVP) release from perifused neurointermediate pituitaries of rats. As opposed to catecholamine-evoked release of peptide, the secretory response to high K⁺ and veratridine involves Ca²⁺ influx, as the effect of both factors was blocked by Ca-chelation and the channel blocker D 600. Leu-enkephalin was found to antagonize AVP secretion induced by K⁺ and veratridine depolarization, by acting through a naloxone-sensitive receptor system. In contrast, the opiate failed to significantly affect isoproterenol-stimulated release of AVP, which we show to be correlated to cAMP accumulation in pure neurohypophyseal tissue. These results support the view that opiates modulate AVP secretion triggered by depolarization of nerve terminals by regulating Ca²⁺ fluxes.