In VivoHypothalamic Release of Thyrotropin-Releasing Hormone after Electrical Stimulation of the Paraventricular Area: Comparison between Push-Pull Perfusion Technique and Collection of Hypophysial Portal Blood

Endocrinology ◽  
1989 ◽  
Vol 125 (2) ◽  
pp. 971-975 ◽  
Author(s):  
J. M. M. RONDEEL ◽  
W. J. DE GREEF ◽  
P. D. M. VAN DER VAART ◽  
P. VAN DER SCHOOT ◽  
T. J. VISSER
Keyword(s):  
Electrical Stimulation ◽  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Perfusion Technique ◽  
Releasing Hormone ◽  
Hypophysial Portal ◽  
Stimulation Of

Is thyrotropin-releasing hormone immunoreactivity in peripheral blood an estimate for hypothalamic thyrotropin-releasing hormone release?

1992 ◽  
Vol 126 (3) ◽  
pp. 276-281 ◽  
Author(s):  
Wim J de Greef ◽  
Jan MM Rondeel ◽  
Rogier Heide ◽  
Wim Klootwijk ◽  
Theo J Visser
Keyword(s):  
Peripheral Blood ◽  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Hormone Release ◽  
Experimental Conditions ◽  
Releasing Hormone ◽  
Two Peaks ◽  
Hypophysial Portal ◽  
Stimulation Of

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.

Interrelationship between Thyroxine and Estradiol on the Secretion of Thyrotropin-Releasing Hormone and Dopamine into Hypophysial Portal Blood in Ovariectomized-Thyroidectomized Rats

1994 ◽  
Vol 59 (3) ◽  
pp. 202-207 ◽  
Author(s):  
Paulus S. Wang ◽  
Seng-Wong Huang ◽  
Yuh-Fan Tung ◽  
Hsiao-Fung Pu ◽  
Shiow-Chwen Tsai ◽  
...  
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Releasing Hormone ◽  
Hypophysial Portal

Effect of Thyroid Status and Paraventricular Area Lesions on the Release of Thyrotropin-Releasing Hormone and Catecholamines into Hypophysial Portal Blood

Endocrinology ◽  
1988 ◽  
Vol 123 (1) ◽  
pp. 523-527 ◽  
Author(s):  
J. M. M. RONDEEL ◽  
W. J. DE GREEF ◽  
P. VAN DER SCHOOT ◽  
B. KARELS ◽  
W. KLOOTWIJK ◽  
...  
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Thyroid Status ◽  
Releasing Hormone ◽  
Hypophysial Portal

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
Keyword(s):  
Electrical Stimulation ◽  
Vasoactive Intestinal Peptide ◽  
Peripheral Blood ◽  
Oestrous Cycle ◽  
Portal Blood ◽  
Female Rats ◽  
Female Wistar Rats ◽  
Consistent Increase ◽  
Hypophysial Portal ◽  
Stimulation Of

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

Enhancement of Immunoreactive Somatostatin Release into Hypophysial Portal Blood by Electrical Stimulation of the Preoptic Area in the Rat*

Endocrinology ◽  
1979 ◽  
Vol 105 (6) ◽  
pp. 1416-1418 ◽  
Author(s):  
KAZUO CHIHARA ◽  
AKIRA ARIMURA ◽  
CARLOS KUBLI-GARFIAS ◽  
ANDREW V. SCHALLY
Keyword(s):  
Electrical Stimulation ◽  
Preoptic Area ◽  
Portal Blood ◽  
Hypophysial Portal ◽  
Stimulation Of

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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