Inhibition by prostaglandin E2of the release of vasopressin and β-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro

1985 ◽  
Vol 106 (2) ◽  
pp. 189-195 ◽  
Author(s):  
W. Knepel ◽  
D. Nutto ◽  
M. Vlaskovska ◽  
Ch. Kittel

ABSTRACT The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells. J. Endocr. (1985) 106, 189–195

1983 ◽  
Vol 96 (3) ◽  
pp. 395-400 ◽  
Author(s):  
S. W. J. Lamberts ◽  
E. G. Bons ◽  
P. Uitterlinden ◽  
W. H. Hackeng

Cyproheptadine and its metabolite desmethylcyproheptadine were shown to suppress directly the release of adrenocorticotrophin (ACTH) and β-lipotrophin/β-endorphin activity from the neurointermediate lobe of the pituitary gland incubated in vitro. Neither compound affected the release of ACTH from the anterior pituitary gland. Serotonin stimulated the release of ACTH and β-lipotrophin/β-endorphin activity from the neurointermediate lobe, but did not influence the (desmethyl)cyproheptadine-mediated inhibition of hormone release. These results indicate that serotonin and cyproheptadine affect hormone release by the neurointermediate lobe by a direct action. The effect of cyproheptadine, however, might not be exerted by a serotonin receptor.


1976 ◽  
Vol 70 (2) ◽  
pp. 197-205 ◽  
Author(s):  
A. P. SCOTT ◽  
P. J. LOWRY ◽  
TJ. B. VAN WIMERSMA GREIDANUS

SUMMARY At least seven radioactive peptides, which fractionated on Biogel P6, were found in rat neurointermediate lobes after incubation for 6 h with [14C]proline. Only three of these could be tentatively identified; one as α-melanocyte-stimulating hormone (α-MSH) and two as forms of corticotrophin-like intermediate lobe peptide (CLIP). One other crossreacted partially with a β-melanocyte-stimulating hormone (β-MSH) antiserum, was acidically charged and eluted on Biogel P6 in roughly the same position as ACTH. The other three peptides showed no resemblance to α-MSH, CLIP, β-MSH or ACTH.


1976 ◽  
Vol 68 (2) ◽  
pp. 283-287 ◽  
Author(s):  
BRIDGET I. BAKER

SUMMARY Various agents were tested for their ability to oppose the stimulatory effect of dibutyryl cyclic AMP on the release of the melanocyte-stimulating hormone from the rat neuro-intermediate lobe in vitro. Only dopamine exhibited an inhibitory effect; serotonin, γ-aminobutyric acid, tocinoic acid, tocinamide, the tripeptide Pro-Leu-Gly-NH2 and dibutyryl cyclic GMP were all ineffective.


1981 ◽  
Vol 97 (3) ◽  
pp. 343-351 ◽  
Author(s):  
F.J. H. Tilders ◽  
M. Post ◽  
S. Jackson ◽  
P.J. Lowry ◽  
P. G. Smelik

Abstract. The intermediate lobe of the rat pituitary gland produces a series of peptides related to ACTH and LPH. The spontaneous and isoproterenol-stimulated release of such peptides was studied during in vitro superfusion of rat neurointermediate lobes with Krebs-Ringer medium. Products released into the superfusion medium were quantified by direct measurement or after chromatography on Sephadex G-50. ACTH bioactivity was determined by use of adrenal cortical cell suspension assay. In addition, NH2-terminal ACTH, CO2H-terminal ACTH, α-MSH and β-endorphin radioimmunoassays were used. The results show that 1. neurointermediate lobes of rats secrete spontaneously various ACTH- and LPH-related peptides in amounts proportional to the amounts in which these peptides are found in extracts of the neurointermediate lobe; 2. the β-adrenergic agonist, isoproterenol, stimulated the spontaneous release of various peptides, including α-MSH, ACTH, CLIP, glycosylated CLIP, and β-endorphin-like peptides; 3. isoproterenol induced a dose-dependent (10−9–10−7 m), parallel increase in the release of α-MSH and ACTH following similar time courses and showing indentical EC50 values (about 10−8 m). Although the spontaneous release of α-MSH and ACTH from rat neurointermediate lobes is not strictly coupled under the conditions used in this study, isoproterenol seems to affect the spontaneous release of these peptides to the same relative extent.


1988 ◽  
Vol 251 (3) ◽  
pp. 503-509 ◽  
Author(s):  
N. B�ck ◽  
K. Salminen ◽  
T. Laatikainen

1989 ◽  
Vol 120 (5) ◽  
pp. 682-688 ◽  
Author(s):  
G. Morel ◽  
J.-G. Chabot ◽  
A. Enjalbert ◽  
M. Priam ◽  
P. M. Dubois

Abstract. Classic concepts of calcitonin (CT) function have focused on the effects of CT on calcium homeostasis. More recently CT actions on brain and pituitary have been investigated. In order to evaluate the effects of CT on the anterior pituitary gland we studied the action(s) of CT in vitro and visualized endogenous CT in adult male rat pituitary gland by immunocytochemistry on ultrathin sections obtained by cryoultramicomy. In vitro study using dispersed anterior pituitary cells indicated that CT stimulated the secretion of PRL, whereas the secretion of GH, TSH and LH was not affected. CT-like immunoreactivity was observed in lactotropes only. The other pituitary cell types were not immunoreactive. In lactotropes, immunostaining was observed in the cytoplasm and in the nucleus. In the cytoplasm, CT-like immunoreactivity was visuzalized in the cytoplasmic matrix and in the secretory granules. In the nucleus, immunostaining was distributed primarly in the euchromatin, in the vincinity of heterochromatin region. CT-like immunoreactivity was also observed at the plasma membrane but was only scarce. No reaction product was found when anti-CT serum pre-incubated with CT was used. In conclusion, these results bring evidence for a direct action of CT on lactotrope regulation in vitro as well as in intact animals.


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