scholarly journals The demonstration of luteinizing hormone releasing factor in hypophysial portal blood of pro-oestrous and hypophysectomized rats

1967 ◽  
Vol 191 (2) ◽  
pp. 407-416 ◽  
Author(s):  
G. Fink ◽  
R. Nallar ◽  
W. C. Worthington
Keyword(s):  
Luteinizing Hormone ◽  
Portal Blood ◽  
Hypophysectomized Rats ◽  
Hypophysial Portal

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

Endopeptidase EC 3.4.24.15 Presence in the Rat Median Eminence and Hypophysial Portal Blood and its Modulation of the Luteinizing Hormone Surge

1997 ◽  
Vol 9 (11) ◽  
pp. 813-822 ◽  
Author(s):  
T. J. Wu ◽  
Adrian R. Pierotti† ◽  
Moshe Jakubowski‡ ◽  
W. John Sheward ◽  
Marc J. Glucksman ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Median Eminence ◽  
Portal Blood ◽  
Luteinizing Hormone Surge ◽  
Hypophysial Portal

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

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

Studies on Spermatogenesis in Rats. III. Effects of Hormonal Treatment on Differentiation Kinetics of the Spermatogenic Cycle in Regressed Hypophysectomized Rats

1971 ◽  
Vol 49 (7) ◽  
pp. 768-775 ◽  
Author(s):  
V. L. W. Go ◽  
R. G. Vernon ◽  
I. B. Fritz
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Hormonal Treatment ◽  
Testicular Function ◽  
Carnitine Acetyltransferase ◽  
Hormonal Replacement ◽  
Hypophysectomized Rats ◽  
Kinetics Of ◽  
Stimulating Hormone

The general hormonal requirements for the restoration of spermatogenesis in regressed hypophysectomized rats were investigated. With the aid of the Staput fractionation technique, it was established that thymidine-3H was readily incorporated into spermatogonia and resting spermatocytes. Labeled cells did not progress to form appreciable numbers of primary spermatocytes or spermatids in the absence of hormonal replacement. The inhibition of formation of pachytene primary spermatocytes in hypophysectomized rats was overcome by administration of follicle-stimulating hormone (FSH), luteinizing hormone (LH), or testosterone, but a combination of either FSH plus LH, or FSH plus testosterone, was required for the progression of pachytene primary spermatocytes to spermatids and spermatozoa. Carnitine acetyltransferase (CAT) measurements in testes from various groups of animals provided ancillary evidence consistent with the conclusion that either FSH, LH, or testosterone was required for the normal restoration of pachytene-diplotene spermatocyte formation. However, one or more additional blocks in spermatogenesis existed in hypophysectomized animals, since elevation of depressed testicular CAT levels in hypophysectomized rats to normal levels required FSH plus LH, or FSH plus testosterone. Cortisone and thyroxin treatment had no measurable effects on testicular function in hypophysectomized rats.

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