Responses to prolactin secretagogues in oestrogen-treated rats suggest that the defect in prolactin regulation produced by oestrogen is at the level of the pituitary gland

1985 ◽  
Vol 104 (3) ◽  
pp. 447-452 ◽  
Author(s):  
J. O. Willoughby ◽  
H. Pederick ◽  
P. Jervois ◽  
M. Menadue ◽  
S. J. Judd
Keyword(s):  
Receptor Blockade ◽  
Pharmacological Agents ◽  
Thyrotrophin Releasing Hormone ◽  
Dopaminergic Activity ◽  
Endogenous Dopamine ◽  
Pituitary Hyperplasia ◽  
Oestradiol Benzoate ◽  
Hypothalamic Control ◽  
Prolactin Response ◽  
High Doses

ABSTRACT Prolactin responses to pharmacological agents were used to characterize the defect in prolactin regulation which occurs after administration of high doses of oestrogen to rats. Animals with chronically implanted venous cannulae were injected with 2 mg oestradiol benzoate in oil and 2–3 days later prolactin concentrations were measured after injections of saline, thyrotrophin-releasing hormone (TRH), fenfluramine, apomorphine and butaclamol. The responses were compared with those in oil-injected animals. Hyperprolactinaemia in oestrogen-treated animals was unresponsive to apomorphine, but was even more sensitive to dopamine receptor blockade than controls. These results suggest that the lactotrophs in oestrogen-treated animals are already maximally suppressed by endogenous dopamine, though ineffectively. Although there was an increased prolactin response to TRH in oestrogen-treated animals, there was an impaired response to fenfluramine, indicating suppressed serotonergic prolactin-releasing factor mechanisms. Maximal endogenous dopaminergic activity and suppressed prolactin-releasing factor mechanisms are appropriate hypothalamic responses to hyperprolactinaemia. The operation of these responses in the earliest stages of the development of pituitary hyperplasia indicates that oestrogen induces a disturbance of prolactin regulation in the lactotroph, independent of hypothalamic control. J. Endocr. (1985) 104, 447–452

Sustained oestrogen-induced hyperprolactinaemia results from a pituitary defect

1983 ◽  
Vol 99 (3) ◽  
pp. 477-483 ◽  
Author(s):  
J. O. Willoughby ◽  
H. J. Pederick ◽  
P. M. Jervois ◽  
M. F. Menadue
Keyword(s):  
Plasma Concentrations ◽  
Male Rats ◽  
Right Atrial ◽  
Complete Suppression ◽  
Thyrotrophin Releasing Hormone ◽  
Intravenous Injections ◽  
Inhibitory Mechanisms ◽  
Pituitary Hyperplasia ◽  
Pituitary Glands ◽  
Prolactin Response

Pituitary enlargement and hyperprolactinaemia were induced in male rats by a single subcutaneous injection of 2 mg oestradiol benzoate in oil. Two months after treatment, when oestrogen levels were normal, serial blood samples for determination of plasma concentrations of prolactin were obtained from undisturbed animals through an indwelling right atrial cannula which had been implanted 7–10 days before. Basal concentrations of prolactin were obtained in treated and control rats, and responses of prolactin to intravenous injections of thyrotrophin releasing hormone (TRH), apomorphine, butaclamol and fenfluramine were measured. Sustained hyperprolactinaemia with pituitary hyperplasia was achieved in only 20% of animals. Responses of prolactin to TRH were the same in control, oestrogen-treated hyperprolactinaemic and non-hyperprolactinaemic rats, indicating normal pituitary responsiveness to one prolactin releasing factor. Complete suppression of prolactin concentrations by apomorphine occurred in hyperprolactinaemic animals, whereas no suppression could be demonstrated in animals with normal (low) basal prolactin levels, indicating good responsiveness of hyperplastic pituitary glands to dopamine inhibition. Dopamine receptor blockade by butaclamol resulted in a vigorous prolactin response in animals with sustained hyperprolactinaemia, indicating that dopaminergic prolactin inhibitory mechanisms remain qualitatively intact, but the response was quantitatively less than in controls, suggesting insufficient hypothalamic release of dopamine. Responses of prolactin to certain doses of fenfluramine were completely abolished in hyperprolactinaemic animals, indicating diminished sensitivity of serotoninergic prolactin releasing factor mechanisms. Prolactin releasing factor unresponsiveness and relative insufficiency of dopaminergic activity could be regarded as physiologically appropriate responses to chronic hyperprolactinaemia. Thus oestrogen-induced chronic hyperprolactinaemia appears to be entirely of pituitary origin.

EFFECTS OF SEROTONIN ON SPONTANEOUS OVULATION: A THEORY FOR THE DUAL HYPOTHALAMIC CONTROL OF OVULATION

1971 ◽  
Vol 68 (2) ◽  
pp. 334-344 ◽  
Author(s):  
Anant P. Labhsetwar
Keyword(s):  
Serotoninergic System ◽  
Dual Control ◽  
Inhibitory Effects ◽  
Catecholaminergic System ◽  
Peripheral Mechanism ◽  
Ovulation Inhibition ◽  
Oestradiol Benzoate ◽  
Hypothalamic Control ◽  
Specific Antagonist

ABSTRACT In an attempt to study the inhibitory effects of serotonin on spontaneous ovulation, the monoamine was administered subcutaneously to rats with 4-day oestrous cycles. Administration (50 mg/kg) at 5.00 p. m. on the day before pro-oestrus interfered with ovulation without affecting vaginal cornification, uterine ballooning or mating. This effect on ovulation could be overcome with methysergide, a specific antagonist of serotonin. Administration, at appropriate times, of LH or oestradiol benzoate or the stimulus provided by mating prevented the inhibitory effects of serotonin. implicating a central rather than a peripheral mechanism in interference with ovulation. This was further confirmed by the persistence in the serotonin-treated animals of high levels of pituitary LH, comparable to pro-oestrous levels. It is probable that serotonin blocked ovulation by augmenting the inhibitory effects of serotoninergic fibres in the hypothalamus. It is postulated on the basis of the present results and those reported in the literature that the hypothalamus exercises a dual control over ovulation, inhibitory influences being transmitted through serotonin-linked neurones while stimulatory effects are delivered via catecholaminergic fibres to neurones which synthesize releasing factor(s) for the ovulating hormone. It is postulated that a certain degree of balance in favour of the catecholaminergic system is necessary for the occurrence of ovulation. Inhibition of ovulation occurs whenever the serotoninergic system gains dominance over catecholaminergic system. The theory can account for the effects on ovulation of a multitude of chemically diverse agents reported in the literature.

Dopaminergic efferent inhibition of carotid body chemoreceptors in chronically hypoxic cats

1984 ◽  
Vol 247 (1) ◽  
pp. R24-R28 ◽  
Author(s):  
S. Lahiri ◽  
N. Smatresk ◽  
M. Pokorski ◽  
P. Barnard ◽  
A. Mokashi ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Dopamine Antagonist ◽  
Receptor Blockade ◽  
Endogenous Dopamine ◽  
Efferent Inhibition ◽  
O2 Partial Pressure ◽  
Haloperidol Treatment ◽  
Carotid Body Chemoreceptors

The observations that the dopamine concentration of the carotid body and efferent inhibition of carotid chemoreceptors are increased during chronic hypoxia led to the hypothesis that the inhibition was due to the effect of an increased dopamine release by the activity of carotid sinus nerve (CSN) efferents. The hypothesis was tested by measuring the effect of dopamine receptor blockade on efferent inhibition of carotid chemosensory responses to graded levels of arterial O2 partial pressure in chronically hypoxic and normoxic cats. Chronically hypoxic cats were prepared by exposing the cats to 10% O2 at sea level for 30–34 days. Carotid chemosensory activity was first measured from a slip of an otherwise intact CSN. The measurements were then repeated after sectioning the remaining nerve trunk. The effect of sectioning the CSN provided the measure of efferent inhibition. In each group of cats the effects of sectioning the CSN with and without dopamine receptor blockade by haloperidol were also studied. CSN section augmented the chemosensory responses in the chronically hypoxic cats. Haloperidol, a dopamine antagonist, augmented the responses further, indicating that a part of the endogenous dopamine effect was independent of the CSN efferents. After haloperidol treatment CSN section did not influence the chemosensory responses. This study confirmed that the efferent inhibition significantly increased in the chronically hypoxic cats and demonstrated that haloperidol blocked the efferent inhibition, suggesting that the mechanism of the augmented inhibition is dopaminergic.

scholarly journals Evaluation of GnRH administration on the prolactin response to thyrotrophin-releasing hormone in normal women.

1986 ◽  
Vol 33 (4) ◽  
pp. 511-517 ◽  
Author(s):  
HISANORI MINAKAMI ◽  
KOZO KIMURA ◽  
KUNIHIKO IJIMA ◽  
AKIO AKABORI ◽  
TARO TAMADA
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Normal Women ◽  
Prolactin Response

Metabolic effects of low and high doses of insulin during beta-receptor blockade in dogs

1985 ◽  
Vol 5 (5) ◽  
pp. 469-478 ◽  
Author(s):  
Olav Reikerås ◽  
Pål Gunnes ◽  
Dag Sørlie ◽  
Rolf Ekroth
Keyword(s):  
Metabolic Effects ◽  
Receptor Blockade ◽  
Beta Receptor ◽  
Beta Receptor Blockade ◽  
High Doses

Parkinson’s disease: Is there a role for dietary and herbal supplements?

2021 ◽  
Vol 20 ◽  
Author(s):  
Olakunle J. Onaolapo ◽  
Ademola O. Odeniyi ◽  
Adejoke Y. Onaolapo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dietary Supplements ◽  
Herbal Remedies ◽  
Key Factors ◽  
Herbal Supplements ◽  
Pharmacological Agents ◽  
Dopaminergic Pathway ◽  
High Doses ◽  
Nigrostriatal Dopaminergic Pathway

: Parkinson’s disease (PD) is characterised by degeneration of the neurons of the nigrostriatal dopaminergic pathway of the brain. The pharmacological cornerstone of PD management is mainly the use of dopamine precursors, dopamine receptor agonists, and agents that inhibit biochemical degradation of dopamine. While these drugs initially relief symptoms and improve the quality of life of patients, progression of the underlying pathological processes such as oxidative stress and neuroinflammation (which have been strongly associated with PD and other neurodegenerative disorders) eventually reduces their benefits; making further benefits now only achievable at high doses which amplify the magnitude and frequency of side-effects. Also, while it is becoming obvious that mainstream pharmacological agents may not always provide the much-needed answer, the question remains what succour can nature provide through dietary supplements, nutraceuticals and herbal remedies? This narrative review examines current literature for evidence of the possible roles (if any) of nutraceuticals, dietary supplements and herbal remedies in the prevention or management of PD, by examining how these compounds could modulate key factors and pathways that are crucial to the pathogenesis and/or progression of PD. The likely limitations of this approach and its possible future roles in PD prevention and management are also considered.

Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men

1995 ◽  
Vol 133 (4) ◽  
pp. 457-462 ◽  
Author(s):  
Inmyung Yang ◽  
Jeongtaek Woo ◽  
Sungwoon Kim ◽  
Jinwoo Kim ◽  
Youngseol Kim ◽  
...  
Keyword(s):  
Internal Medicine ◽  
Growth Hormone ◽  
Large Dose ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
School Of Medicine ◽  
Prolactin Response ◽  
Normal Men ◽  
Different Doses

Yang I, Woo J, Kim S, Kim J, Kim Y, Choi Y. Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men. Eur J Endocrinol 1995;133:457–62. ISSN 0804–4643 Pyridostigmine (PST), a cholinesterase inhibitor, induces a clear growth hormone (GH) release in man by suppression of hypothalamic somatostatin (SRIH). Somatostatin suppresses thyrotrophin (TSH) release in rats and men. Earlier studies showed that the thryotrophin-releasing hormone (TRH)-induced TSH response was not altered by 60–120 mg of PST. We studied whether a larger dose (180 mg) of PST can increase the TSH response to TRH. Six healthy young men were studied with the following six tests: (Test 1) 200 μg of TRH iv; (Test 2) 180 mg of PST po; (Test 3) three different doses of PST (60, 120, 180 mg) + TRH; (Test 4) 100 μg of octreotide (SMS) iv; (Test 5) SMS + TRH; (Test 6) PST + SMS + TRH. A large dose of PST (180 mg) significantly augmented GH, TSH and prolactin responses to TRH, while smaller doses of PST (60 and 120 mg) did not significantly increase the responses of GH and TSH. While the increased TRH-induced prolactin response by PST was not suppressed by SMS, the increased responses of GH and TSH were suppressed remarkably by SMS. Most of the subjects noticed a mild to moderate abdominal pain, nausea and muscular fasciculation after the administration of a large dose of PST administration. These data suggest that suppression of hypothalamic SRIH secretion by 180 mg of PST can augment the TSH response to TRH. However, the considerable side effects should be minimized before clinical application of the combined PST–TRH test. Inmyung Yang, Division of Endocrinology, Department of Internal Medicine, Kyunghee University School of Medicine, 1 Hoiki-dong, Dongdaemoon-ku, Seoul, 130–702, Korea

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