VASOPRESSIN POTENTIATES CYCLIC AMP ACCUMULATION AND ACTH RELEASE INDUCED BY CORTICOTROPIN-RELEASING FACTOR (CRF) IN RAT ANTERIOR PITUITARY CELLS IN CULTURE

Endocrinology ◽  
1982 ◽  
Vol 111 (5) ◽  
pp. 1752-1754 ◽  
Author(s):  
VINCENT GIGUERE ◽  
FERNAND LABRIE
Keyword(s):  
Cyclic Amp ◽  
Anterior Pituitary ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Cells In Culture ◽  
Anterior Pituitary Cells ◽  
Cyclic Amp Accumulation ◽  
Acth Release

Regulation of ACTH secretory pathways in cultured pituitary cells

1991 ◽  
Vol 261 (5) ◽  
pp. C793-C798 ◽  
Author(s):  
J. Schwartz ◽  
S. Gibson ◽  
A. White
Keyword(s):  
Anterior Pituitary ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Receptor Complex ◽  
Response Mechanism ◽  
Acth Secretion ◽  
Secretory Pathways ◽  
Anterior Pituitary Cells ◽  
Acth Release

Although chloroquine, an agent that disrupts regulated protein secretion, has previously been shown to decrease the adrenocorticotropic hormone (ACTH) secretory response to adenosine 3',5'-cyclic monophosphate or corticotropin-releasing factor (CRF) in AtT-20 and rat anterior pituitary cells, respectively, it has no effect on the response to vasopressin. The present study extended experiments with chloroquine to cultured sheep anterior pituitary cells, which have a greater maximum response to vasopressin. Chloroquine (200 microM) had no effect on basal ACTH secretion or on stimulation by vasopressin. In contrast to the rat, the net response to CRF was tripled by chloroquine in ovine cells. The effect of chloroquine on the response to CRF was more effective by coexposure of cells to CRF and chloroquine than by pretreatment with chloroquine. Monensin or vinblastine did not increase the ACTH response to CRF. The results indicate ACTH release in response to vasopressin is chloroquine insensitive in this way, can be dissociated from the mechanism that responds to CRF, and would be consistent with the CRF response mechanism involving pathways that can alter the secretory pool of ACTH. When chloroquine acts to increase the response to CRF, it is likely not to act by stabilizing the CRF-receptor complex.

scholarly journals Cocaine- and Amphetamine-Regulated Transcript Activates the Hypothalamic-Pituitary-Adrenal Axis through a Corticotropin-Releasing Factor Receptor-Dependent Mechanism

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5202-5209 ◽  
Author(s):  
Sean M. Smith ◽  
Joan M. Vaughan ◽  
Cynthia J. Donaldson ◽  
Jean Rivier ◽  
Chien Li ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Anterior Pituitary ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Hypothalamic Pituitary Adrenal ◽  
Anterior Pituitary Cells ◽  
Circulating Levels ◽  
Dependent Mechanism ◽  
Acth Release

Abstract Cocaine- and amphetamine-regulated transcript (CART) is a highly expressed hypothalamic transcript that is concentrated in areas associated with the stress response. There is evidence for a role of CART in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis. However, it is not clear whether CART regulates activity of the HPA axis by directly stimulating ACTH release from pituitary corticotropes or through interaction with hypothalamic factors. To address this issue, the effects of central and peripheral administration of CART on the HPA axis were compared. Central administration of CART(55–102) (1 μg) significantly increased circulating levels of ACTH (481 ± 122 vs. 93 ± 14 pg/ml; CART vs. vehicle) and corticosterone (460 ± 29 vs. 179 ± 62 ng/ml; CART vs. vehicle). In contrast, iv injection of CART(55–102) (0.09-9.0 nmol/kg) did not significantly affect circulating levels of ACTH or corticosterone. The corticotropin-releasing factor (CRF) receptor antagonist Astressin B was used to determine whether CART(55–102) elicits ACTH secretion via a CRF receptor-dependent mechanism. Injection of Astressin B (50 μg/kg, iv) inhibited CART(55–102)-induced ACTH and corticosterone responses. The effects of CART(55–102) on CRF and arginine vasopressin (AVP) expression were also examined in static hypothalamic explants. RT-PCR analysis revealed a significant up-regulation of CRF and AVP mRNA levels after CART(55–102) (10 nm and 1 μm) treatment. Last, the effects of CART(55–102) on CRF- and AVP-mediated ACTH release was investigated in dispersed rat anterior pituitary cells. Incubation of CART(55–102) (10–100 nm) did not significantly affect ACTH release from anterior pituitary cells. Findings from the present study suggest that CART regulates activity of the HPA axis through a CRF-dependent central mechanism and not by means of direct interaction with pituitary corticotropes.

The effect of nifedipine on CRF-41 and AVP-induced ACTH release in vitro

1985 ◽  
Vol 109 (1) ◽  
pp. 32-36 ◽  
Author(s):  
Kazuharu Murakami ◽  
Kozo Hashimoto ◽  
Zensuke Ota
Keyword(s):  
Cyclic Amp ◽  
Calcium Ions ◽  
Anterior Pituitary ◽  
Inhibitory Effect ◽  
Extracellular Calcium ◽  
Pituitary Cells ◽  
Amp System ◽  
Cyclic Amp Accumulation ◽  
Acth Release

Abstract. The effect of nifedipine on CRF-41- and AVP-induced ACTH release was examined using monolayer cultured rat anterior pituitary cells and pituitary halves. Nifedipine inhibited ACTH release induced by synthetic rat CRF-41 in two systems. In pituitary halves, CRF-41 significantly stimulated both ACTH release and cyclic AMP accumulation. Nifedipine inhibited CRF-41-induced ACTH release and the inhibitory effect of nifedipine on CRF-41-induced ACTH release was accompanied by parallel decrease of cyclic AMP levels in pituitary halves. Nifedipine did not inhibit AVP-induced ACTH release in pituitary halves, and AVP did not significantly affect cyclic AMP accumulation in pituitary halves. These results suggest that CRF-41 stimulates ACTH release through the intracellular cyclic AMP system and calcium-calmodulin system which are accelerated by the influx of extracellular calcium ions. Moreover, it is suggested that the calcium required for AVP-induced ACTH release is derived primarily from intracellular rather than extracellular sources.

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