Arginine Vasopressin Is a Much More Potent Stimulus to ACTH Release from Ovine Anterior Pituitary Cells than Ovine Corticotropin-Releasing Factor

1989 ◽  
Vol 50 (2) ◽  
pp. 152-157 ◽  
Author(s):  
Mary Familari ◽  
Ian Smith ◽  
Robin Smith ◽  
John W. Funder
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
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 effects of corticotrophin-releasing hormone, arginine vasopressin and their antagonists on ACTH release from perifused horse anterior pituitary cells

1994 ◽  
Vol 143 (1) ◽  
pp. 85-93 ◽  
Author(s):  
M J Ellis ◽  
R S Mulligan ◽  
M J Evans ◽  
R A Donald
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Dose Range ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
The Individual ◽  
Acth Release

Abstract Antagonists are useful for probing hormone action and receptor characteristics. In this study we have investigated the inhibitory effects of analogues of arginine vasopressin (AVP) and corticotrophin-releasing hormone (CRH) on stimulated release of immunoreactive ACTH from perifused equine anterior pituitary cells in vitro. Our aims were to gain some insight into the characteristics of the CRH and AVP receptors of the horse pituitary and to establish whether the response induced by AVP and CRH together could be blocked by combining antagonists. Experimental design included 5-min pulses of AVP (12·5 nmol/l), CRH (0·3 nmol/l) or CRH plus AVP given every 40 min alternately with pulses of secretagogue(s) plus appropriate antagonist(s). The effect of combined antagonists on the response to lower secretagogue concentrations (CRH, 0·03 nmol/l plus AVP, 2·5 nmol/l) was also tested. Response in the presence of an antagonist was compared with the mean response to secretagogue in the immediately preceding and following pulse and was expressed as per cent expected ACTH. The ACTH response to AVP was inhibited over the dose range 0·4–50 μmol/l by Phaa-d-Tyr(Et)2Lys6Arg3VP (P<0·002; ANOVA) and by d(CH2)5[Tyr(Me)2]AVP (P<0·001). Suppression of the expected ACTH response to AVP by these two antagonists was most effectively achieved by antagonist concentrations of 10 μmol/l (to 28±2·1%) and 25 μmol/l (to 22±5·1%) respectively. Inhibition was not improved by preinfusion compared with a bolus pulse. Aaa-d-Tyr(Et)2Val4Abu6Arg8·9VP and the non-peptide antagonist OPC-21268 had no inhibitory effect. Two α-helical (α-h) analogues of CRH, (α-hCRH(12–41) and α-hCRH(9–41) tested over the dose range 0·5–5 μmol/l, suppressed CRH-induced ACTH secretion (P<0·001) but CRH(23–41) had no significant effect. The α-hCRH(12–41) achieved greater suppression of ACTH release than the (9–41) derivative (8·7±4·2% compared with 19·3±3·5% of the expected ACTH response). Combination of d(CH2)5[Tyr(Me)2]AVP (25 μmol/l) plus α-hCRH (12–41) (5·0 μmol/l) achieved suppression to −0·5±1·3% and 0·8±1·5% of the expected response to CRH+AVP at 0·3+12·5 nmol/l and 0·03+2·5 nmol/l respectively. These effects were greater than seen by the individual antagonists alone. The antagonist effects suggest that the CRH and AVP receptors of the equine pituitary have similar properties to those from other species and are consistent with the pituitary AVP receptor being unlike the V2 receptor and resembling but not being identical to the V1 type. We also conclude that α-hCRH(12–41) and d(CH2)5[Tyr(Me)2]AVP can together block the ACTH response to CRH plus AVP and suggest that these antagonists should provide a means of investigating additional secretagogues involved in ACTH release in the horse. Journal of Endocrinology (1994) 143, 85–93

scholarly journals Desensitization of the adrenocorticotrophin responses to arginine vasopressin and corticotrophin-releasing hormone in ovine anterior pituitary cells

2003 ◽  
Vol 178 (3) ◽  
pp. 491-501 ◽  
Author(s):  
A Hassan ◽  
S Chacko ◽  
D Mason
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Prolonged Exposure ◽  
No Reduction ◽  
Pituitary Cells ◽  
Acth Secretion ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells

Following repeated or prolonged exposure to either corticotrophin-releasing hormone (CRH) or arginine vasopressin (AVP), pituitary adrenocorticotrophin (ACTH) responsiveness is reduced. This study compared the characteristics of desensitization to CRH and AVP in perifused ovine anterior pituitary cells. Desensitization to AVP occurred at relatively low AVP concentrations and was both rapid and readily reversible. Treatment for 25 min with AVP at concentrations greater than 2 nM caused significant reductions in the response to a subsequent 5 min 100 nM AVP pulse (IC(50)=6.54 nM). Significant desensitization was observed following pretreatment with 5 nM AVP for as briefly as 5 min. Desensitization was greater following a 10 min pretreatment, but longer exposures caused no further increase. Resensitization was complete within 40 min following 15 min treatment with 10 nM AVP. Continuous perifusion with 0.01 nM CRH had no effect on AVP-induced desensitization. Treatment with 0.1 nM CRH for either 25 or 50 min caused no reduction in the response to a subsequent 5 min stimulation with 10 nM CRH. When the pretreatment concentration was increased to 1 nM significant desensitization was observed, with a greater reduction in response occurring after 50 min treatment. Recovery of responsiveness was progressive following 50 min treatment with 1 nM CRH and was complete after 100 min. Our data show that in the sheep AVP desensitization can occur at concentrations and durations of AVP exposure within the endogenous ranges. This suggests that desensitization may play a key role in regulating ACTH secretion in vivo. If, as has been suggested, CRH acts to set corticotroph gain while AVP is the main dynamic regulator, any change in responsiveness to CRH may significantly influence the overall control of ACTH secretion.

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