Hypothalamic catecholaminergic effects on prolactin release in vitro

1978 ◽  
Vol 56 (2) ◽  
pp. 304-309 ◽  
Author(s):  
W. C. Friend ◽  
G. M. Brown ◽  
S. Kirpalani ◽  
D. Wilson

Hypothalamic catecholaminergic influences on prolactin release were investigated in vitro. Both dopamine and norepinephrine caused long lasting inhibition of prolactin release from either an isolated hemipituitary or a hemipituitary coincubated with a hypothalamus. Epinephrine also inhibited prolactin release. L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. DL-Threodihydroxyphenylserine (threodops), serotonin, 5-hydroxy-L-tryptophan (5-HTP), tyramine, octopamine, synephrine, thyrotropin-releasing hormone (TRH), luteinizing hormone releasing hormone (LH-RH), and somatostatin all failed to alter prolactin release. Results confirm that dopamine and norepinephrine directly inhibit prolactin release from pituitary and suggest that the hypothalamic mechanism inhibiting prolactin involves dopamine but not norepinephrine.

1976 ◽  
Vol 82 (3) ◽  
pp. 706-709 ◽  
Author(s):  
Gwyneth E. Jones ◽  
A. R. Boyns

ABSTRACT Anterior canine pituitaries were maintained in tissue culture for 8 days, and the immunoreactive prolactin released, was measured by a heterologous radioimmunoassay for canine prolactin. Luteinizing hormone-releasing hormone (LH-RH) and thyrotrophic hormone-releasing hormone (TRH) did not affect prolactin release, while theophylline and oestradiol-17β stimulated the release of canine prolactin.


1977 ◽  
Vol 75 (2) ◽  
pp. 277-283 ◽  
Author(s):  
N. BARDEN ◽  
A. BETTERIDGE

The addition of luteinizing hormone releasing hormone (LH-RH) to cultures of monolayers of rat anterior pituitary cells was shown to increase both the concentrations of prostaglandins E1 and E2 (PGE) in the cells and the release of LH over similar ranges of concentrations of LH-RH (10−6 to 10−10 mol/l). The peak concentration of PGE was observed after 2·5 h. The stimulation of the level of PGE in the cells by LH-RH was completely inhibited by two inhibitors of prostaglandin synthetase, which only partially inhibited the stimulation of LH release. Therefore the increased concentration of PGE was not obligatory for the effect of LH-RH on LH release. It was also shown that monobutyryl cyclic AMP stimulated the intracellular concentration of PGE and it is suggested that the stimulation of PGE levels may be mediated by increased levels of cyclic AMP in the cells after the addition of LH-RH.


1976 ◽  
Vol 68 (2) ◽  
pp. 197-207 ◽  
Author(s):  
J. A. EDWARDSON ◽  
D. GILBERT

SUMMARY A technique is described for the continuous perifusion of rat adenohypophyses. Exposure of the perifused glands to repeated equal 5 min stimuli with hypothalamic extract resulted in a series of equal peaks of corticotrophin secretion, the response was proportional to log dose over the range 0·25–2·0 rat hypothalamic equivalents/ml. Repeated equal stimuli with hypothalamic extract, or with luteinizing hormone releasing hormone (LH-RH) at concentrations of 2 or 10 ng/ml, resulted in a progressively increasing series of peaks of LH secretion, i.e. a self-potentiating or priming effect. The effect took between 30 min and 1 h to develop. A delayed increase in the responsiveness of the glands was also seen with continuous incubation of anterior pituitaries with LH-RH. The relevance of these observations to the physiological control of LH secretion is discussed.


1979 ◽  
Vol 57 (12) ◽  
pp. 1388-1392 ◽  
Author(s):  
M. Fevre ◽  
D. Jordan ◽  
J. Tourniaire ◽  
R. Mornex

The mechanism of action of adiphenine on in vitro rat anterior pituitary LH release was studied and compared with that of the physiological stimulator luteinizing hormone releasing hormone (LH-RH) on LH release. The comparative study showed that adiphenine and LH-RH were able to increase medium LH concentration in a dose-dependent manner and had similar time courses of action between 1 and 4 h incubation. However, there were several main differences between the effects of adiphenine and LH-RH. The adiphenine action was not calcium dependent, was inhibited in a high K+ medium concentration, and was substituted after energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the LH release pathway and could be a useful pharmacological tool for studying the mechanism of LH release.


1976 ◽  
Vol 5 (s1) ◽  
pp. s279-s289 ◽  
Author(s):  
L. FERLAND ◽  
F. LABRIE ◽  
M. SAVARY ◽  
M. BEAULIEU ◽  
D.H. COY ◽  
...  

1979 ◽  
Vol 80 (1) ◽  
pp. 141-152 ◽  
Author(s):  
A. D. SWIFT ◽  
D. B. CRIGHTON

The abilities of three nonapeptide analogues of synthetic luteinizing hormone releasing hormone (LH-RH) to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in anoestrous and cyclic ewes were examined, as were their elimination from the plasma in vivo and degradation by extracts of the hypothalamus, anterior pituitary gland, lung, kidney, liver and plasma in vitro. In all cases, comparisons were made with synthetic LH-RH. When injected i.v. into mature ewes as a single dose, the potencies of the analogues were graded and Des Gly-NH210 LH-RH ethylamide was found to be the least potent. It was not possible to demonstrate any significant increase in the potency of this analogue over LH-RH, although a trend was apparent with each parameter examined. [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide had the greatest potency. There were no differences between the responses of anoestrous ewes and those of ewes treated on day 10 of the oestrous cycle. None of the analogues had a rate of elimination from the plasma different from that of LH-RH during either the first or the second components of the biphasic disappearance curve. The incubation of LH-RH with tissue extracts showed that extracts of the hypothalamus and anterior pituitary gland degraded LH-RH to a similar extent. Both the hypothalamic and anterior pituitary gland extracts degraded more LH-RH than did lung extract, which in turn destroyed more LH-RH than did extracts of kidney or liver tissue. The degradative abilities of kidney and liver extracts did not differ from each other. Plasma failed to degrade LH-RH or the analogues. Although LH-RH was rapidly destroyed by hypothalamic extract in vitro, of the analogues, only Des Gly-NH210 LH-RH ethylamide was degraded. The anterior pituitary gland and kidney extracts failed to degrade [d-Ser6] Des Gly-NH210 LH-RH ethylamide and [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide as rapidly as LH-RH. Extracts of liver and lung were incapable of catabolizing any of the analogues. There was an inverse correlation between the LH- and FSH-releasing potency of an analogue and its rate of degradation by anterior pituitary gland extract. The slower rates of catabolism of certain analogues of LH-RH by the anterior pituitary gland may explain their increased LH- and FSH-releasing potency.


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