Vasoactive intestinal peptide in rat hypophysial portal blood: effects of electrical stimulation of various brain areas, the oestrous cycle and anaesthetics

1985 ◽  
Vol 106 (3) ◽  
pp. 275-280 ◽  
Author(s):  
A. K. Brar ◽  
G. Fink ◽  
M. Maletti ◽  
W. Rostene

ABSTRACT Vasoactive intestinal peptide (VIP) was measured by radioimmunoassay in hypophysial portal and peripheral blood from adult male and female Wistar rats. The results confirmed that the concentration of VIP in hypophysial portal blood was significantly greater than in peripheral blood and showed that VIP release into portal blood was not affected by removal of the gut, the largest peripheral source of VIP. Electrical stimulation of the median eminence, several hypothalamic nuclei, the amygdala or hippocampus had no significant effect on the release of VIP into portal blood, possibly because under the conditions of the experiment the spontaneous release of VIP is already at a maximum. In female rats, the VIP released into portal blood collected between 13.00 and 18.30 h of each day of the 4-day oestrous cycle varied under different anaesthetics, and there was no consistent increase in VIP release on pro-oestrus suggesting that VIP is not involved in the pro-oestrous surge of prolactin. J. Endocr. (1985) 106, 275–280

1992 ◽  
Vol 126 (3) ◽  
pp. 276-281 ◽  
Author(s):  
Wim J de Greef ◽  
Jan MM Rondeel ◽  
Rogier Heide ◽  
Wim Klootwijk ◽  
Theo J Visser

The significance of TRH for pituitary function is still unresolved mainly due to limitations in determining in vivo hypothalamic TRH release. We therefore examined whether TRH immunoreactivity (TRH-IR) in peripheral blood is an index for hypothalamic TRH release. Peripheral TRH-IR varied between 10 and 55 pmol/l and was similar in euthyroid and hypothyroid rats, but lower in hyperthyroid rats. Destruction of the hypothalamic paraventricular area reduced peripheral TRH-IR, while stimulation of this area increased it. Clearance of TRH during continuous TRH infusion was 1.9±0.2, 3.5±0.3 and 5.9±0.8 ml/min in hypothyroid, euthyroid and hyperthyroid rats, respectively. These and previous data on TRH in hypophysial portal blood indicate that 5–25 pmol TRH/I peripheral blood is of hypothalamic origin. Chromatography revealed that TRH-IR from hypothalamus and portal blood co-eluted with TRH, but in peripheral blood two peaks were found, one of which was authentic TRH. Thus, peripheral TRH-IR alters in experimental conditions and part of it seems to be of hypothalamic origin. However, the presence of TRH-like material in peripheral blood not identical to TRH and the fact that experimental conditions alter TRH clearance indicate that peripheral TRH-IR is not an index for hypothalamic TRH release.


1985 ◽  
Vol 104 (2) ◽  
pp. 211-NP ◽  
Author(s):  
A. M. Horn ◽  
I. C. A. F. Robinson ◽  
G. Fink

ABSTRACT Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation. The concentrations of OT and VP in portal blood are sufficiently high for these peptides to play a significant role in neural control of the anterior pituitary gland. J. Endocr. (1985) 104, 211–224


Endocrinology ◽  
1979 ◽  
Vol 105 (6) ◽  
pp. 1416-1418 ◽  
Author(s):  
KAZUO CHIHARA ◽  
AKIRA ARIMURA ◽  
CARLOS KUBLI-GARFIAS ◽  
ANDREW V. SCHALLY

1991 ◽  
Vol 129 (1) ◽  
pp. 99-107 ◽  
Author(s):  
L. A. Tannahill ◽  
W. J. Sheward ◽  
I. C. A. F. Robinson ◽  
G. Fink

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


1976 ◽  
Vol 68 (1) ◽  
pp. 71-87 ◽  
Author(s):  
G. FINK ◽  
M. G. JAMIESON

SUMMARY Blood was collected from the cut pituitary stalk of male and female rats before and during the application of an electrical stimulus to the medial preoptic area. The plasma was assayed for immunoreactive LH releasing factor (RF) by a double antibody radioimmunoassay using a specific antiserum raised in rabbits against the free acid derivative of the decapeptide LH-RF conjugated to bovine serum albumin. The decapeptide (used as a standard) and pituitary stalk plasma cross-reacted in a similar manner with the antiserum. Stimulation of the preoptic area increased significantly the amount of LH-RF in pituitary stalk plasma in both male and female rats. The increase in LH-RF was linearly related to the strength of the stimulating current, and the amount of LH-RF liberated diminished on cessation of the stimulus. The concentration of LH-RF in pituitary stalk plasma from female rats was significantly greater than that in jugular venous plasma. The magnitudes of the mean increments of LH-RF in pituitary stalk plasma (stimulation minus pre-stimulation values) at various times of the oestrous cycle in female rats suggests that between 18.00 h of dioestrus and 13.00 h of pro-oestrus there is an increase in sensitivity of the LH-RF secretory mechanism to electrical stimulation. However, the increments decreased in magnitude between 13.00 and 18.00 h of pro-oestrus, indicating that the marked increase in responsiveness of the hypothalamo-hypophysial system to electrical stimulation which occurs during this period is due mainly to a change in sensitivity of the pituitary gonadotrophs to LH-RF. The LH-RF in pituitary stalk plasma collected before application of the stimulus was higher at some of the times examined during pro-oestrus than at other times of the oestrous cycle. A higher level of the secretion of the factor may be important for the full development of the priming effect of LH-RF and, consequently, the marked increase in responsiveness of the pituitary gland which occurs during the afternoon of pro-oestrus.


1962 ◽  
Vol 39 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roger A. Gorski ◽  
Charles A. Barraclough

ABSTRACT We have previously suggested that the failure of the androgen-sterilized, persistent-oestrous rat to ovulate, following electrical stimulation of the median eminence structures of the hypothalamus, is due to an insufficiency in adenohypophyseal LH concentration. Using the ovarian ascorbic acid technique for quantitative determination of pituitary LH content, the present studies have demonstrated that the sterile rat pituitary gland contains one-third the LH content of the normal prooestrous gland. Furthermore, not only does progesterone priming of this persistent-oestrous rat result in a 75 % increase in LH concentration, but on hypothalamic stimulation sufficient LH is released to induce ovulation. The decrease in LH concentration which accompanies ovulation in the progesterone-primed, sterile rat is approximately 45 % of the total gland content as compared with a 51 % decrease in pituitary content in the normal cyclic rat.


1974 ◽  
Vol 75 (3) ◽  
pp. 569-578 ◽  
Author(s):  
G. Buffler ◽  
S. Roser

ABSTRACT The mechanisms involved in the prolongation of the oestrous cycle following LH administration were studied in 4-day cyclic female Wistar rats. In females injected with LH on the morning of dioestrus I there was an increase in ovarian venous blood progesterone as compared with non-injected animals. In both LH-treated females, and those injected with progesterone on the morning of dioestrus I, a slowing up in follicular growth was observed from the afternoon of dioestrus I. The size of follicles greater than 400 urn present in LH or progesterone injected animals on the third day of cycle was similar to the size reached by the same range of follicles in non-injected animals on the second day of the cycle. Hence, the increase in endogenous ovarian progesterone elicited by LH was considered as the cause of the slowing up of follicular growth and therefore of the lengthening of the oestrous cycle duration in female rats injected with LH at the beginning of 4-day cycle.


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