Role of arginine vasopressin and corticotropin-releasing factor in mediating alcohol-induced adrenocorticotropin and vasopressin secretion in male rats bearing lesions of the paraventricular nuclei

1997 ◽  
Vol 744 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Kathleen M Ogilvie ◽  
Soon Lee ◽  
Catherine Rivier
2018 ◽  
Vol 237 (2) ◽  
pp. 207-216
Author(s):  
Hiroshi Nagano ◽  
Yuki Sobue ◽  
Hayato Matsuyama ◽  
Shoichiro Saito ◽  
Hiroki Sakai ◽  
...  

Muscarinic acetylcholine receptors have been suggested to be implicated in arginine–vasopressin secretion because intracerebroventricular muscarinic agonist administration induces arginine–vasopressin release into the circulation. Although which subtype is involved in the regulation of arginine–vasopressin secretion is unclear, M2 receptors have been reported to be highly expressed in the hypothalamus. In the present study, M2 receptor-knockout mice were used to elucidate whether M2 receptor regulates arginine–vasopressin synthesis in the paraventricular nuclei and supraoptic nuclei of the hypothalamus. The number of arginine–vasopressin-immunoreactive neurons in M2 receptor-knockout mice was significantly decreased in the supraoptic nuclei, but not in the paraventricular nuclei compared with wild-type mice. Plasma arginine–vasopressin level in M2 receptor-knockout mice was also significantly lower than in the wild-type mice. Urinary volume and frequency as well as water intake in M2 receptor-knockout mice were significantly higher than those in wild-type mice. The V2 vasopressin receptor expression in kidneys of M2 receptor-knockout mice was comparable with that of wild-type mice, and increased urination in M2 receptor-knockout mice was significantly decreased by administration of desmopressin, a specific V2 receptor agonist, suggesting that V2 receptors in the kidneys of M2 receptor-knockout mice are intact. These results suggest that M2 receptors promote arginine–vasopressin synthesis in the supraoptic nuclei and play a role in the regulation and maintenance of body fluid.


Neuroreport ◽  
1997 ◽  
Vol 8 (5) ◽  
pp. 1277-1281 ◽  
Author(s):  
J Wayte ◽  
J C. Buckingham ◽  
A M. Cowell

1992 ◽  
Vol 127 (5) ◽  
pp. 435-440 ◽  
Author(s):  
B Conte-Devolx ◽  
V Guillaume ◽  
F Boudouresque ◽  
N Graziani ◽  
E Magnan ◽  
...  

The effects of rapid changes of circulating cortisol levels on ACTH secretion and on corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) concentrations into hypophysial portal blood were studied in six adult rams. Pharmacological adrenalectomy was obtained by 3 h metyrapone infusion (100 mg·kg−1·h−1). Blockade of cortisol synthesis induced a tenfold increase of plasma ACTH levels accompanied by a moderate increase of CRF secretion (150% vs preinjection levels) and a large increment of AVP secretion (535% vs preinjection levels). ACTH levels remained high during the 3 h following the end of metyrapone infusion. During the same period, CRF secretion was still elevated (231% vs preinjection levels), while AVP secretion was further stimulated (2,151% vs preinjection levels). Subsequent hydrocortisone infusion (66 μg·kg−1·h−1) for 2 h induced a rapid decrease of both ACTH and AVP secretion, while CRF levels in hypophysial portal blood still remained elevated. These data suggest that changes in ACTH secretion induced by acute modifications of the negative glucocorticoid feedback are, in addition to the well documented direct effect of cortisol on the corticotropes, mainly mediated by variations of hypothalamic AVP secretion.


2006 ◽  
Vol 291 (1) ◽  
pp. R29-R36 ◽  
Author(s):  
Inga D. Neumann ◽  
Luz Torner ◽  
Nicola Toschi ◽  
Alexa H. Veenema

In response to forced swimming (FS), AVP is released somato-dendritically within the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but not from neurohypophyseal terminals into blood. Together with AVP, oxytocin (OXT) is released within the SON and PVN. Here, we studied the role of intra-SON and intra-PVN OXT in the regulation of local AVP release and into the blood in male rats. Within the SON, bilateral retrodialysis of an OXT receptor antagonist (OXT-A) increased local AVP release in response to FS [60 s, 21°C, vehicle twofold, not significant (ns); OXT-A: 15-fold increase, P < 0.05] without significantly affecting basal AVP release. In addition, local OXT-A elevated plasma AVP secretion under basal conditions (twofold increase, P < 0.05) without further elevation after FS. Within the PVN, exposure to FS elevated local AVP release, reaching significance only in the OXT-A group (vehicle: 1.4-fold, ns; OXT-A: 1.6-fold increase, P = 0.050). Bilateral OXT-A into the PVN did not affect peripheral AVP secretion either under basal or stress conditions. Basal ACTH concentrations tended to be elevated by local OXT-A within the PVN (1.7-fold increase, P = 0.076). In contrast, the swim-induced ACTH secretion was attenuated after retrodialysis of OXT-A within both the SON (at 5 min) and PVN (at 15 min) ( P < 0.05 both) compared with vehicle. The results demonstrate a receptor-mediated effect of OXT within the SON and PVN on local and neurohypophyseal AVP release, which depends upon the activity conditions. Further, while exerting an inhibitory effect on hypothalamo-pituitary-adrenal axis activity under basal conditions, hypothalamic OXT is essential for an adequate acute ACTH response.


1983 ◽  
Vol 244 (3) ◽  
pp. R363-R367 ◽  
Author(s):  
A. J. Baertschi ◽  
J. L. Beny ◽  
G. B. Makara

To study the role of the paraventricular nucleus and of neurohypophysial hormones in the control of ACTH secretion, the paraventricular nuclei (PV) of Brattleboro diabetes insipidus rats (DI) were lesioned (L) with a knife; sham-lesioned DI (S) served as controls. Four days later, the rats were stressed by ether inhalation, and blood samples were taken during and 30–40 min after stress for the determination of corticosterone. The median eminence (ME) and neural lobe (NL) were homogenized in 50 microliters of 0.1 N HCl and frozen pending bioassay of corticotropin-releasing factor (CRF). PV lesion almost abolished the corticosterone secretion to ether and reduced the ME CRF content three- to sevenfold. The NL CRF content in S was about twice that of ME, and oxytocin accounted for more than 60% of NL CRF. However, PV lesion had no effect on NL CRF activity. Low amounts of oxytocin (2 mU/ml) had no significant CRF activity but potentiated the ME CRF effect in L. The results suggest that 1) PV is one of the most important sites for CRF synthesis or CRF fiber transit in DI; 2) corticosterone secretion to ether stress is governed mainly by ME CRF; and 3) a large proportion of CRF fibers to NL probably originates outside PV.


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