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

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

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

Concentrations of dopamine and noradrenaline in hypophysial portal blood in the sheep and the rat

1989 ◽  
Vol 121 (1) ◽  
pp. 141-147 ◽  
Author(s):  
G. B. Thomas ◽  
J. T. Cummins ◽  
G. A. Smythe ◽  
R. M. Gleeson ◽  
R. C. Dow ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Portal Blood ◽  
Female Rats ◽  
Male Rats ◽  
Gas Chromatography Mass Spectrometry ◽  
Intact Male ◽  
Peripheral Plasma ◽  
Portal Plasma ◽  
Urethane Anaesthesia ◽  
Hypophysial Portal

ABSTRACT The concentrations of dopamine, noradrenaline and their respective primary neuronal metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylethyleneglycol (DHPG) were measured in the hypophysial portal and peripheral plasma of sheep and rats by combined gas chromatography–mass spectrometry. Hypophysial portal and jugular blood samples were taken at 5- to 10-min intervals for 3–7 h from six conscious ovariectomized ewes. Blood was also collected for 30 min under urethane anaesthesia from the cut pituitary stalk from 16 pro-oestrous female and five intact male rats. In ovariectomized ewes, noradrenaline concentrations were higher in hypophysial portal plasma than in peripheral plasma (6·6 ± 0·8 vs 2·2 ± 0·4 nmol/l). In contrast, dopamine was undetectable (<1 nmol/l) in the portal and peripheral plasma of all ewes. Plasma levels of DOPAC and DHPG in portal and jugular samples were similar. In all pro-oestrous female rats, plasma concentrations of dopamine were higher in portal blood than in jugular blood (8·0±1·4 vs 4·8± 0·6 nmol/l). Detectable concentrations of dopamine were measured in the portal plasma of two out of five male rats. Noradrenaline concentrations were higher in portal plasma than in peripheral plasma of both female (8·3 ± 1·7 vs 3·7 ± 0·6 nmol/l) and male (14·8± 2·7 vs 6·1± 1·2 nmol/l) rats. These data show that noradrenaline, but not dopamine, is secreted into the long portal vessels in sheep. The results suggest that there are species differences in the secretion of hypothalamic dopamine into hypophysial portal blood. Journal of Endocrinology (1989) 121, 141–147

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

Corticotrophin-releasing factor-41, vasopressin and oxytocin release into hypophysial portal blood in the rat: effects of electrical stimulation of the hypothalamus, amygdala and hippocampus

1991 ◽  
Vol 129 (1) ◽  
pp. 99-107 ◽  
Author(s):  
L. A. Tannahill ◽  
W. J. Sheward ◽  
I. C. A. F. Robinson ◽  
G. Fink
Keyword(s):  
Electrical Stimulation ◽  
Plasma Concentrations ◽  
Direct Proof ◽  
Brain Regions ◽  
Portal Blood ◽  
Male Rats ◽  
Unilateral Stimulation ◽  
Oxytocin Release ◽  
Hypophysial Portal ◽  
Stimulation Of

ABSTRACT The role of the paraventricular nuclei (PVN), amygdala and hippocampus in the control of the hypothalamic-pituitary-adrenal axis has been studied by determining the effect of electrical stimulation of the PVN, amygdala and hippocampus on the release of corticotrophin-releasing hormone (CRF-41) and arginine vasopressin (AVP) into hypophysial portal blood and ACTH and corticosterone into peripheral blood. Adult female Wistar rats were anaesthetized with sodium pentobarbitone and stimulation was carried out through previously implanted bipolar, glass-insulated platinum electrodes. Hypophysial portal blood was collected 30 min before and 30 min during the application of the stimulus which consisted of trains (30 s on and 30 s off) of biphasic rectangular pulses with a frequency of 50 Hz, pulse width 1 ms and amplitude 1 mA. Bilateral stimulation of the PVN increased while unilateral stimulation of the amygdala decreased the release of CRF-41 into hypophysial portal blood. The threefold increase in release of CRF-41 induced by PVN stimulation correlated with a marked increase in peripheral plasma concentrations of ACTH and corticosterone. Stimulation of the hippocampus had no significant effect on CRF-41 release, and stimulation of each of the three brain regions had no effect on AVP release into portal blood. These findings were extended in a second study to compare the effects of unilateral bipolar electrical stimulation of the PVN and of the supraoptic nucleus (SON) on the release of CRF-41, AVP and oxytocin. This study was carried out on adult male rats, anaesthetized with sodium pentobarbitone, in which the stimulus was applied through previously implanted concentric stainless-steel electrodes. Unilateral stimulation of the PVN resulted in a significant increase in the release of CRF-41 and a massive increase in oxytocin release into portal blood. Increased release of oxytocin also occurred after unilateral stimulation of the SON, but CRF-41 secretion was unaffected. The secretion of AVP was unaffected by electrical stimulation of either the SON or PVN. These results (i) provide the first direct proof for the fact that the PVN is the major source of CRF-41 in hypophysial portal blood, and (ii) suggest that the release of CRF-41 may be inhibited by the amygdala. Journal of Endocrinology (1991) 129, 99–107

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