Role for serotonin3 receptors in the control of adrenocorticotropic hormone release from rat pituitary cell cultures

1995 ◽  
Vol 133 (2) ◽  
pp. 251-254 ◽  
Author(s):  
Aldo E Calogero ◽  
Gyorgy Bagdy ◽  
Nunziatina Burrello ◽  
Pietro Polosa ◽  
Rosario D'Agata
Keyword(s):  
Pituitary Gland ◽  
Receptor Antagonist ◽  
Cell Cultures ◽  
Adrenocorticotropic Hormone ◽  
Pituitary Cell ◽  
Hormone Release ◽  
Mdl 72222 ◽  
Rat Pituitary ◽  
Ics 205 930 ◽  
Acth Release

Calogero AE, Bagdy G, Burrello N, Polosa P. D'Agata R. Role for serotonin3 receptors in the control of adrenocorticotropic hormone release from rat pituitary cell cultures. Eur J Endocrinol 1995;133:251–4. ISSN 0804–4643 Although several serotonin (5-HT) receptor types have been shown capable of stimulating the release of adrenocorticotropic hormone (ACTH) from the pituitary gland, relatively little is known about the role of the 5-HT3 receptor, a receptor that has generated a great deal of interest for its involvement in many behavioral and therapeutic effects. Hence, in this study, we tested the effects of the 5-HT¾ receptor antagonist 3-tropanyl-indole-3-carboxylate (ICS 205-930) and the selective 5-HT3 receptor antagonist 3-tropanyl-3,5-dichlorobenzoate (MDL 72222) on ACTH release stimulated by 5-HT from primary cultures of rat pituitary cells. Subsequently, we evaluated the effects of the selective 5-HT3 receptor agonist 1-(m-chlorophenyl)-biguanide (m-CPBG) on basal, corticotropin-releasing hormone (CRH)- and arginine vasopressin (AVP)-stimulated ACTH release. The maximal stimulatory effect of 5-HT (10−9 mol/l on ACTH release was antagonized by both ICS 205-930 and MDL 72222, suggesting that 5-HT stimulates basal ACTH release through activation of 5-HT3 receptors. Accordingly, m-CPBG stimulated basal ACTH release in a concentration-dependent fashion. In contrast to 5-HT, m-CPBG did not have any effect on CRH-stimulated ACTH release and inhibited AVP-stimulated ACTH release in a concentration-dependent manner. These data suggest that the 5-HT3 receptor is involved in the release of ACTH from the pituitary gland in vitro. Aldo E Calogero, Istituto di Clinica Medica I, Ospedale Garibaldi, Piazza S Maria di Gesú, 95123 Catania, Italy

Effects of adrenomedullin on adrenocorticotropic hormone (ACTH) release in pituitary cell cultures and on ACTH and oxytocin responses to shaker stress in conscious rat

2001 ◽  
Vol 922 (2) ◽  
pp. 261-266 ◽  
Author(s):  
Tomoko Mimoto ◽  
Tatsuya Nishioka ◽  
Koichi Asaba ◽  
Toshihiro Takao ◽  
Kozo Hashimoto
Keyword(s):  
Cell Cultures ◽  
Adrenocorticotropic Hormone ◽  
Pituitary Cell ◽  
Conscious Rat ◽  
Acth Release

scholarly journals Effects of Vasopressin V1b Receptor Deficiency on Adrenocorticotropin Release from Anterior Pituitary Cells in Response to Oxytocin Stimulation

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 4883-4891 ◽  
Author(s):  
Kazuaki Nakamura ◽  
Yoko Fujiwara ◽  
Reiko Mizutani ◽  
Atsushi Sanbe ◽  
Noriko Miyauchi ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Receptor Antagonist ◽  
Anterior Pituitary ◽  
Primary Cultures ◽  
Control Level ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
V1b Receptor ◽  
Rat Pituitary ◽  
Acth Release

Oxytocin (OT) is one of the secretagogues for stress-induced ACTH release. OT-induced ACTH release is reported to be mediated by the vasopressin V1b receptor in the rat pituitary gland, which contains both OT and V1b receptors. We examined OT-induced ACTH release using primary cultures of anterior pituitary cells from wild-type (V1bR+/+) and V1b receptor knockout (V1bR−/−) mice. OT stimulated similar levels of ACTH release from pituitary cells of V1bR+/+ and V1bR−/− mice. OT-induced ACTH release was significantly inhibited by the selective V1b receptor antagonist SSR149415 and the OT receptor antagonist CL-14-26 in V1bR+/+ mice. In addition, cotreatment with SSR149415 at 10−6m and CL-14-26 at 10−6m inhibited OT-induced ACTH release to the control level inV1bR+/+ mice. In V1bR−/− mice, OT-induced ACTH release was significantly inhibited by CL-14-26 at 10−8m and completely inhibited at 10−7m. These results indicate that OT induces the ACTH response via OT and V1b receptors inV1bR+/+ mice but via only OT receptors in V1bR−/− mice. The gene expression level of the OT receptor was significantly higher in the anterior pituitary gland of V1bR−/− mice than in that of V1bR+/+ mice, suggesting that the OT receptor is up-regulated to compensate for ACTH release under conditions of V1b receptor deficiency.

Comparison of mitogenic activity of (Bu)2cAMP and different growth factors in rat pituitary cell cultures and the influence on hormone secretion

1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S193
Author(s):  
L. ANGERMÜLLER ◽  
G. K. STALLA ◽  
J. STALLA ◽  
J. MOJTO ◽  
O. A. MÜLLER
Keyword(s):  
Growth Factors ◽  
Cell Cultures ◽  
Hormone Secretion ◽  
Pituitary Cell ◽  
Mitogenic Activity ◽  
Rat Pituitary

Vasopressin-binding sites in the pig pituitary gland: competition by novel vasopressin antagonists suggests the existence of an unusual receptor subtype in the anterior lobe

1994 ◽  
Vol 141 (3) ◽  
pp. 383-391 ◽  
Author(s):  
Y Arsenijevic ◽  
M Dubois-Dauphin ◽  
E Tribollet ◽  
M Manning ◽  
W H Sawyer ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Rat Liver ◽  
Arginine Vasopressin ◽  
Binding Sites ◽  
Anterior Lobe ◽  
Receptor Subtype ◽  
Lower Affinity ◽  
Corticotrophin Releasing Factor ◽  
Rat Pituitary ◽  
Acth Release

Abstract Arginine vasopressin (AVP) acts in the pituitary gland, in synergy with corticotrophin-releasing factor, to induce ACTH release in response to stressful stimuli. Pituitary AVP receptors in the rat are coupled to phospholipase C, as are the so-called V1-type AVP receptors. The present study examined [3H]AVP binding in membranes prepared from the anterior lobe of the pituitary gland of the pig. [3H]AVP, alone or in competition with analogues, bound to sites in the pig anterior lobe which are pharmacologically similar to those described previously by others in the rat pituitary gland. For comparison, the same competition studies were performed on membrane preparations from the rat liver which contain the classic V1-type AVP receptor. Pituitary and liver AVP-binding sites were dissimilar; both cyclic and linear V1 antagonists had, in general, a much lower affinity for pituitary AVP-binding sites than for those in the liver. Thus, Phaa-d-Tyr(Et)-Phe-Gln-Asn-Lys-Pro-Arg-NH2 (Phaa=phenylacetyl) has a 2500-fold greater affinity for the latter (negative logarithm of inhibition constant (pKi)=9·64) than for the former (pKi=6·22). One linear antagonist, Pa-d-Tyr-Phe-Val-Asn-Arg-Pro-Arg-Arg-NH2 (Pa=propionyl) had about equal affinities for liver and pituitary membranes (pKi=6·39 and 6·53 respectively). Another compound, Phaa-d-Tyr-Phe-Val-Asn-Arg-Pro-Arg-Arg-NH2 had the highest affinity found to date for binding to AVP sites in the pituitary (pKi=7·43). These findings suggest some ideas for the design of more potent and/or selective AVP analogues acting in the pituitary gland. Journal of Endocrinology (1994) 141, 383–391

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