Serum Growth Hormone and Prolactin Response to Thyrotropin-Releasing Hormone in Patients with Acromegaly Before and After Surgery

1974 ◽  
Vol 38 (6) ◽  
pp. 957-963 ◽  
Author(s):  
NAGUIB A. SAMAAN ◽  
MILAM E. LEAVENS ◽  
RICHARD H. JESSE
Cephalalgia ◽  
1990 ◽  
Vol 10 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Paola Piccini ◽  
Angelo Nuti ◽  
Anna Maria Paoletti ◽  
Alessandro Napolitano ◽  
Gian Benedetto Melis ◽  
...  

Flunarizine, a calcium antagonist widely used in the prophylactic treatment of migraine, may interfere with dopaminergic systems. Flunarizine therapy can in fact induce extrapyramidal side effects and can increase basal as well as stimulated prolactin levels. To better define the mechanism of flunarizine action in migraine, we studied prolactin and growth hormone responses to thyrotropin releasing hormone and sulpiride in 13 female migraineurs before and after 60 days of flunarizine therapy. The treatment did not modify basal prolactin and growth hormone levels, but prolactin response to thyrotropin releasing hormone was enhanced. A paradoxical increase of growth hormone to thyrotropin releasing hormone observed before therapy was blunted after flunarizine treatment. These data indicate a modulatory action of flunarizine on dopaminergic systems which might to some extent explain the antimigraine action of this drug.


1987 ◽  
Vol 114 (2) ◽  
pp. 275-282 ◽  
Author(s):  
G. R. Rutteman ◽  
R. Stolp ◽  
A. Rijnberk ◽  
S. Loeffler ◽  
J. A. Bakker ◽  
...  

Abstract. Growth hormone (GH), prolactin (Prl) and cortisol secretion was studied in 5 ovariohysterectomized dogs before and after oestradiol implantation and medroxy-progesterone acetate (MPA) administration. MPA was given at regular intervals during a period of 10 months in a total of 12 injections. Short-term effects of oestradiol were restricted to significantly enhanced Prl responses to thyrotropin-releasing hormone (TRH). MPA treatment after oestradiol implantation resulted in significanly elevated basal GH levels in all dogs, with a continuing increase in one dog. Only in the latter dog was a significant decrease in basal Prl levels seen. MPA administration did not significantly change Prl responses to TRH. The GH responses to clonidine were significantly reduced at 9 and 16 weeks of oestradiol and MPA treatment. In the one dog which exhibited the greatest rise in basal GH levels, GH responses were completely abolished at 9, 16 and 43 weeks of oestradiol and MPA treatment. TRH never evoked significant GH responses. Both basal and lysine-vasopressin (LVP)-stimulated cortisol levels were significantly suppressed during combined oestradiol-MPA treatment. These findings denote that in the dog. 1) Oestradiol rapidly induces an enhanced Prl response to TRH. 2) The oestradiol-MPA induced GH overproduction is associated with a reduced responsiveness of GH to clonidine and is not accompanied by GH responsiveness to TRH. 3) Oestradiol-MPA treatment suppresses both basal and LVP-stimulated cortisol secretion.


1977 ◽  
Vol 233 (5) ◽  
pp. E430
Author(s):  
R A Steiner ◽  
P Illner ◽  
P Marques ◽  
D Williams ◽  
L Shen ◽  
...  

The effects of thyrotropin-releasing hormone (TRH) and dopamine (DA) on serum growth hormone (GH) levels were examined in the adolescent male baboon. Intravenously administered DA (40 microgram/kg-min-1 for 20 min) raised serum GH and glucose and lowered serum insulin concentrations but caused no increase in blood pressure. Concomitant intravenous infusion of TRH at 2 doses (96 ng/kg-min-1 and 40 microgram/kg-min-1 for 20 min) blocked the DA-induced increase in serum GH. The relatively low effective doses of TRH used to suppress the DA-induced GH increase suggest an interaction with catecholamines at the hypothalamic and/or pituitary to influence GH release.


1991 ◽  
Vol 71 (4) ◽  
pp. 1045-1052 ◽  
Author(s):  
Peter Løvendahl ◽  
John A. Woolliams ◽  
Patrick A. Sinnett-Smith

Doses of growth hormone releasing factor (GRF) and thyrotropin releasing hormone (TRH) and combinations of these were administered by intravenous injection to six calves aged 155 ± 3 days and weighing 136 ± 16 kg. Injections were at 09:00, 12:00 and 15:00 h on 4 days, and doses were 0, 15, 30 and 60 pmol GRF kg−1 and 0, 275, 550 and 1100 pmol TRH kg−1, with GRF plus TRH at all combinations of these doses. Response of serum growth hormone (GH) was measured as the mean at 5, 10, 15 and 20 min following injection (PEAK) and the area under the curve during 0–60 min (AUC). The correlation between PEAK and AUC was 0.98. The variation in PEAK was related to GH prior to injection and to PEAK 3 h earlier. Separate multiplicative effects for each secretagogue were fitted, with the effects related to the logarithm of dose. Doubling the dose increased PEAK by 1.46-fold following GRF (P < 0.05) and 1.25-fold following TRH (P < 0.05). There was no evidence that the results for either secretagogue were affected by the presence or absence of the other. This multiplicative model provides a description of the synergy between these secretagogues. Key words: GH-release, GRF, TRH, calves, dose response


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