Effects of corticosterone on the secretion of corticotrophin-releasing factor, arginine vasopressin and oxytocin into hypophysial portal blood in long-term hypophysectomized rats

1991 ◽  
Vol 129 (1) ◽  
pp. 91-98 ◽  
Author(s):  
W. J. Sheward ◽  
G. Fink
Keyword(s):  
Arginine Vasopressin ◽  
Portal Blood ◽  
Blood Collection ◽  
Continuous Administration ◽  
Feedback Effects ◽  
Corticotrophin Releasing Factor ◽  
Hypophysectomized Rats ◽  
Hypophysial Portal ◽  
Intact Rats

ABSTRACT To investigate the feedback effects of corticosterone on the secretion of corticotrophin-releasing factor-41 (CRF-41), oxytocin and arginine vasopressin (AVP), hypophysial portal vessel blood was collected from control (intact) and long-term (6–8 weeks) hypophysectomized rats. In preliminary experiments in rats anaesthetized with urethane, long-term hypophysectomy resulted in a significant increase in the secretion of oxytocin and AVP; the hypothalamic contents of oxytocin and AVP were also increased in comparison with pituitary-intact rats. In long-term hypophysectomized rats anaesthetized with sodium pentobarbitone, but not with urethane, the output of CRF-41 into portal blood was increased twofold in comparison with that in control rats. In long-term hypophysectomized rats anaesthetized with pentobarbitone, the i.v. infusion of corticosterone (7·2 nmol/min) for a 2 h period of portal blood collection did not alter the secretion of CRF-41, oxytocin or AVP into portal blood; however, the secretion of CRF-41 and, to a lesser extent, AVP was significantly reduced in hypophysectomized rats by continuous corticosterone replacement, by a pellet of corticosterone implanted s.c. for 5 days before portal blood collection. These results confirm that the secretion of CRF-41 is differently affected by the anaesthetics urethane and pentobarbitone, and in long-term hypophysectomized rats show (i) that there were no apparent feedback effects of corticosterone infusion over a 2 h period on the secretion of any of the peptides studied, (ii) that late delayed feedback effects of continuous administration of corticosterone are mediated by a reduction in CRF-41 and AVP output, and (iii) that corticosterone has no effects on oxytocin secretion into portal blood. Journal of Endocrinology (1991) 129, 91–98

Hypothalamic release of atrial natriuretic factor and β-endorphin into rat hypophysial portal plasma: relationship to oestrous cycle and effects of hypophysectomy

1991 ◽  
Vol 131 (1) ◽  
pp. 113-125 ◽  
Author(s):  
W. J. Sheward ◽  
A. Lim ◽  
B. Alder ◽  
D. Copolov ◽  
R. C. Dow ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Portal Blood ◽  
Female Rats ◽  
Male Rats ◽  
Blood Collection ◽  
Peripheral Plasma ◽  
Portal Plasma ◽  
Hypophysectomized Rats ◽  
Hypophysial Portal

ABSTRACT The release of β-endorphin and atrial natriuretic factor (ANF) into hypophysial portal plasma was investigated in male and female Wistar rats. The principal aim of the study was to investigate the possible role of β-endorphin and ANF in the hypothalamic control of LH and prolactin secretion. In male rats, anaesthetized with urethane, the concentrations of β-endorphin in portal blood collected immediately after hypophysectomy were within the same range as those in peripheral plasma. Furthermore, electrical stimulation of the median eminence did not increase the portal plasma concentrations of β-endorphin. In female rats, anaesthetized with alphaxalone, the portal plasma concentrations in long-term (6–8 weeks) or acutely hypophysectomized rats were significantly greater than those in peripheral plasma. In acutely hypophysectomized female rats the concentrations and contents of β-endorphin in portal plasma collected at 10.00–11.30 h of pro-oestrus were significantly (approximately sixfold) greater than at dioestrus or at 20.00–21.00 h of pro-oestrus, but these changes were not consistently seen in all experiments. In female rats in which the pituitary gland was not removed for portal blood collection, portal plasma contents of ANF remained unchanged throughout the day of pro-oestrus, suggesting that it is unlikely that ANF is involved in the spontaneous LH or prolactin surge. The effects of ovarian steroids on the secretion of hypothalamic ANF and β-endorphin were determined by measuring the portal plasma concentration of ANF and β-endorphin on the morning of presumptive pro-oestrus in rats ovariectomized 24 h previously and injected with either oil or oestradial benzoate (OB). Portal plasma contents of ANF were significantly lower in OB- compared with oil-treated rats, suggesting that oestradiol inhibits ANF release into rat hypophysial portal plasma. In contrast, there were no significant between-group differences in the content or concentration of β-endorphin in portal plasma. Thus, the increased β-endorphin in the portal plasma of some of the intact animals during the morning of pro-oestrus is not due to the preovulatory surge of oestradiol-17β. The output of β-endorphin into portal blood in long-term hypophysectomized rats was lower than in dioestrous or pro-oestrous rats in which the pituitary gland was removed immediately before portal blood collection. Taken together, these results suggest that β-endorphin release into portal plasma may depend upon normal physiological levels of pituitary and pituitary-dependent hormones in the circulation, and that β-endorphin release into portal blood is not controlled by short- or long-loop negative feedback. In sum, these data confirm that in adult female rats, ANF and β-endorphin are released into hypophysial portal plasma and show (i) that the secretion of ANF, but not of β-endorphin, can be affected by oestradiol, (ii) that the concentrations of ANF in portal plasma are sufficient to affect the release of pituitary hormones but are not related to plasma concentrations of LH and prolactin during the afternoon of pro-oestrus, (iii) that whilst there is no simple inverse relationship between βendorphin overflow into portal plasma and LHRH secretion, the increased release of β-endorphin during the morning of pro-oestrus may be consistent with a role for this peptide in triggering the pro-oestrous surge of pro-lactin, and (iv) that a sex difference in β-endorphin release into portal plasma is suggested by the absence of β-endorphin in the portal plasma of male rats. Journal of Endocrinology (1991) 131, 113–125

Release of oxytocin but not corticotrophin-releasing factor-41 into rat hypophysial portal vessel blood can be made opiate dependent

1990 ◽  
Vol 124 (1) ◽  
pp. 141-150 ◽  
Author(s):  
W. J. Sheward ◽  
J. E. Coombes ◽  
R. J. Bicknell ◽  
G. Fink ◽  
J. A. Russell
Keyword(s):  
Portal Blood ◽  
Morphine Dependence ◽  
Opiate Withdrawal ◽  
Portal Vessel ◽  
Peripheral Plasma ◽  
Corticotrophin Releasing Factor ◽  
Intracerebroventricular Infusion ◽  
Oxytocin Release ◽  
Hypophysectomized Rats ◽  
Hypophysial Portal

ABSTRACT The effects of morphine dependence and abrupt opiate withdrawal on the release of oxytocin and corticotrophin-releasing factor-41 (CRF-41) into hypophysial portal vessel blood in rats anaesthetized with urethane were investigated. Adult female Sprague–Dawley rats were made dependent upon morphine by intracerebroventricular infusion of morphine for 5 days; abrupt opiate withdrawal was induced by injection of the opiate antagonist naloxone. The basal concentrations of oxytocin in portal or peripheral plasma from morphine-dependent rats did not differ significantly from those in control, vehicle-infused rats. In rats in which the pituitary gland was not removed after stalk section, the i.v. injection of naloxone hydrochloride (5 mg/kg) resulted in a large and sustained increase in the concentration of oxytocin in both portal and peripheral plasma in control and morphine-dependent rats. The i.v. injection of naloxone resulted in a threefold increase in the secretion of oxytocin into portal blood in acutely hypophysectomized rats infused with morphine, but did not alter oxytocin secretion in vehicle-infused hypophysectomized rats. The concentration of oxytocin in peripheral plasma in both vehicle- and morphine-infused hypophysectomized rats was at the limit of detection of the assay and was unchanged by the administration of naloxone. There were no significant differences in the secretion of CRF-41 into portal blood in vehicle- or morphine-infused hypophysectomized rats either before or after the administration of naloxone. These data show that, as for oxytocin release from the neurohypophysis into the systemic circulation, the mechanisms which regulate oxytocin release into the portal vessel blood can also be made morphine dependent. The lack of effect of morphine or naloxone on the release of CRF-41 or other stress neurohormones suggests that the effect of opiate dependence and withdrawal is selective for oxytocin and is not simply a non-specific response to 'stress'. Journal of Endocrinology (1990) 124, 141–150

Mechanism of restoration of ACTH release in rats with long-term lesions of the paraventricular nuclei

1986 ◽  
Vol 111 (1) ◽  
pp. 75-82 ◽  
Author(s):  
J. Dohanics ◽  
G. Kapócs ◽  
T. Janáky ◽  
J. Z. Kiss ◽  
G. Rappay ◽  
...  
Keyword(s):  
Median Eminence ◽  
Plasma Concentrations ◽  
Plasma Acth ◽  
Corticotrophin Releasing Factor ◽  
Paraventricular Nuclei ◽  
Basal Plasma ◽  
Corticosterone Response ◽  
Intact Rats ◽  
Acth Release

ABSTRACT The effects of lesions in the paraventricular nucleus (PVN) on the adrenocortical response to ether stress were investigated in neurohypophysectomized and intact rats. During the first 4 days after placement of lesions in the PVN, the corticosterone response to ether stress was almost completely inhibited. It then gradually increased and, within 4–6 weeks of surgery, was restored to about 60% of that in sham-operated rats. Basal plasma concentrations of corticosterone were low in rats after placement of lesions in the PVN and/or after neurointermediate lobectomy (NILX). Corticosterone responses to ether stress were similar in groups submitted to PVN lesions and/or NILX, and lower than those in the appropriate sham-operated groups. In all lesioned groups, plasma ACTH concentrations after a combination of stressors (ether plus laparotomy) were also lower than those in the sham-operated groups. Six weeks after lesioning of the PVN, immunoreactive rat corticotrophin-releasing factor-41 (rCRF-41) concentrations in stalk-median eminence (SME) extract fell to about 5% of that in sham-operated rats, while immunoreactive arginine vasopressin (AVP) concentrations did not change. Immunohistochemistry revealed a substantial decrease in rCRF-41 immunostaining of the median eminence 6 weeks after lesioning of the PVN, though randomly located clusters of stained terminals were still seen in the whole rostro-caudal extent of the median eminence. A mixture containing synthetic rCRF-41 and AVP, in proportions similar to those in SME extracts from sham-operated rats, caused significantly less release of ACTH from anterior pituitary cell cultures than did SME extracts from sham-operated rats. Extracts of SME from PVN-lesioned rats released as much ACTH as a mixture containing synthetic rCRF-41 and AVP in proportions similar to those in the SME extracts from PVN-lesioned rats. Extracts of SME from either PVN-lesioned or sham-operated rats did not cause a significant increase in the amount of ACTH released when preincubated with antisera to both rCRF-41 and AVP. It is suggested that (1) the restoration of the adrenocortical reponse to ether stress, evident within a few days of placement of lesions in the PVN, occurs independently of neurohypophysial function; (2) the full corticosterone and ACTH response to ether or ether plus laparotomy stress requires not only an intact PVN but also an intact neurointermediate lobe; (3) SME extracts from sham-operated rats contain a factor(s) with the ability to potentiate the ACTHreleasing effect of rCRF-41 and AVP; and (4) the ACTH-releasing activity of SME extract obtained from rats with long-term PVN lesions is probably due to its remaininJ content of rCRF-41 and AVP. J. Endocr. (1986) 111, 75–82

Corticotrophin-releasing peptides in rat hypophysial portal blood after paraventricular lesions: a marked reduction in the concentration of corticotrophin-releasing factor-41, but no change in vasopressin

1990 ◽  
Vol 125 (2) ◽  
pp. 175-183 ◽  
Author(s):  
F. A. Antoni ◽  
G. Fink ◽  
W. J. Sheward
Keyword(s):  
Median Eminence ◽  
Feedback Inhibition ◽  
Portal Blood ◽  
Corticotrophin Releasing Factor ◽  
Paraventricular Nuclei ◽  
Oxytocin Release ◽  
Male Wistar Rats ◽  
Hypophysial Portal ◽  
Supraoptic Nuclei

ABSTRACT Previous data show that corticotrophin-releasing factor-41 (CRF-41), arginine vasopressin (AVP) and oxytocin are released into hypophysial portal blood. It has been presumed that the CRF-41 originates mainly from parvicellular neurones of the paraventricular nuclei (PVN); however, AVP and oxytocin could also be derived as a consequence of preterminal release from magnocellular projections to the neurohypophysis. The latter has been suggested to be the case for AVP as assessed by studies of the median eminence in vitro. Here we have investigated the source of CRF-41, AVP and oxytocin in hypophysial portal blood of adult male Wistar rats 8–10 days after surgical lesioning of the PVN. In PVN-lesioned animals the output of CRF-41 into hypophysial portal blood was reduced by about 90%, and that of oxytocin by about 40%: however, the output of AVP into portal blood was reduced only by about 10%. The release of AVP into portal blood increased after adrenalectomy; this increased release could be returned to normal by treatment with dexamethasone. No change of AVP release occurred after adrenalectomy in animals in which the PVN had been lesioned. These results show (i) that most of the CRF-41 released into hypophysial portal blood is derived from the PVN, (ii) that in PVN-lesioned animals AVP and oxytocin release remains at near normal or 60% of normal respectively, suggesting that a substantial amount of both neuropeptides in portal blood is derived as a consequence of preterminal release from supraoptic nuclei projections in the median eminence, and (iii) that glucocorticoid feedback inhibition of AVP release is exerted at the level of the PVN. Journal of Endocrinology (1990) 125, 175–183

Corticotrophin Releasing Factor in Hypophysial Portal Blood of Rats

Nature ◽  
1971 ◽  
Vol 230 (5294) ◽  
pp. 467-468 ◽  
Author(s):  
G. FINK ◽  
JANICE R. SMITH ◽  
J. TIBBALLS
Keyword(s):  
Portal Blood ◽  
Corticotrophin Releasing Factor ◽  
Hypophysial Portal

Activation of pituitary-adrenal function in fetal sheep by corticotrophin-releasing factor and arginine vasopressin

1990 ◽  
Vol 124 (1) ◽  
pp. 27-35 ◽  
Author(s):  
A. N. Brooks ◽  
A. White
Keyword(s):  
Negative Feedback ◽  
Arginine Vasopressin ◽  
Plasma Concentrations ◽  
Premature Delivery ◽  
Fetal Sheep ◽  
Feedback Effects ◽  
Adrenal Axis ◽  
Corticotrophin Releasing Factor ◽  
Endogenous Cortisol ◽  
Pituitary Adrenal Axis

ABSTRACT In sheep, birth is preceded by an increase in fetal plasma concentrations of ACTH and cortisol. Activation of the fetal pituitary-adrenal axis is pivotal to the onset of parturition in this species and may be regulated, at least in part, by corticotrophin-releasing factor (CRF). Pulsed administration of CRF has been shown to activate the fetal pituitary-adrenal axis in immature fetal sheep. However, pituitary ACTH responsiveness declined after continued administration of CRF, as a result of increasing negative feedback effects of increased concentrations of endogenous cortisol. To test the hypothesis that arginine vasopressin (AVP) is required, in addition to CRF, to produce the necessary trophic stimulus to the pituitary-adrenal axis, we administered saline, CRF (1 μg), AVP (200 ng) or CRF plus AVP as pulses every 4 h for 7 days to fetal sheep beginning at days 117–120 of pregnancy (term =145 days). Pituitary-adrenal responses were assessed by measuring plasma concentrations of immunoreactive (ir) ACTH and cortisol in response to one of the pulses on each of the 7 days of treatment. On day 1, CRF and AVP significantly increased plasma concentrations of ir-ACTH and there was a synergistic interaction when the two peptides were given together (P<0·05). However, as pulsed treatment continued there was a decline in the pituitary ir-ACTH response to all treatments (P<0·05). This decline in pituitary response occurred over a much longer period of time when CRF and AVP were given together when compared with the two peptides given separately. In contrast, the cortisol response to endogenously released ir-ACTH after administration of CRF, AVP or CRF plus AVP was small on day 1 but gradually increased as treatment progressed. This was particularly apparent when the two peptides were given together. A significant inverse correlation (r = 0·781, P<0·01) between basal cortisol concentrations and the ir-ACTH response to CRF plus AVP was observed over the 7 days of treatment. Premature delivery was not induced by any of the treatments despite significant increases in fetal adrenal weight. Furthermore, there were no changes in the circulating maternal plasma concentrations of progesterone or oestrone during the 7 days of the experiment. We conclude that combination of CRF and AVP administered as pulses to immature fetal sheep results in a greater degree of pituitary-adrenal activation when compared with the two peptides given independently. However, even after this combined treatment regimen pituitary responsiveness eventually declines, an effect which may be due to increased negative feedback effects of increased endogenous cortisol. Journal of Endocrinology (1990) 124, 27–35

Effects of metyrapone infusion on corticotropin-releasing factor and arginine vasopressin secretion into the hypophysial portal blood of conscious, unrestrained rams

1992 ◽  
Vol 127 (5) ◽  
pp. 435-440 ◽  
Author(s):  
B Conte-Devolx ◽  
V Guillaume ◽  
F Boudouresque ◽  
N Graziani ◽  
E Magnan ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Corticotropin Releasing Factor ◽  
Portal Blood ◽  
Moderate Increase ◽  
Acth Secretion ◽  
Tenfold Increase ◽  
Rapid Changes ◽  
Vasopressin Secretion ◽  
Large Increment ◽  
Hypophysial Portal

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.

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