Effects of Desipramine Treatment upon Central Adrenoceptor Function in Normal Subjects

1984 ◽  
Vol 145 (2) ◽  
pp. 139-145 ◽  
Author(s):  
T. H. Corn ◽  
C. Thompson ◽  
S. A. Checkley

SummarySix normal subjects were given clonidine infusions after 0, 1 and 3 weeks of treatment with desipramine (2 mg/kgm) and at 1 and 3 weeks after withdrawal from desipramine. The sedative and hypotensive effects of clonidine were inhibited after one and three weeks of desipramine treatment, and returned to normal after stopping treatment without any rebound increase. Such a time-course can be explained in terms of the acute effects of the drug, no adaptive changes at receptors need be invoked.By contrast, the growth hormone response to clonidine tended to be increased after one week of desipramine, reduced after three weeks of treatment, and further reduced after discontinuation. Such a time-course is consistent with an adaptive down regulation at α2 adrenoceptors in response to their acute stimulation, due to noradrenaline re-uptake blockade.

1970 ◽  
Vol 39 (5) ◽  
pp. 663-674 ◽  
Author(s):  
N. W. Oakley ◽  
H. S. Jacobs ◽  
R. C. Turner ◽  
J. Williams ◽  
C. Dos ◽  
...  

1. Hypoglycaemia induces glucose intolerance in normal subjects—the ‘Somogyi effect’–and may be responsible for some instances of ‘brittle diabetes’. This effect may be mediated through the growth hormone response to hypoglycaemia, but other possible hormonal mechanisms have not been excluded. 2. Paired 2-h oral glucose tolerance tests have been carried out 2 h after both (a) i.v. saline (control day) and (b) i.v. insulin (test day) in four normal subjects and twenty-seven patients with pituitary and adrenal under- and over-activity. Plasma glucose, insulin, Cortisol and growth hormone have been estimated at half-hourly intervals during the 4 h of each study. 3. A significant Somogyi effect is usually seen only when there is a growth hormone response to insulin-induced hypoglycaemia; hypopituitary subjects do not show the effect. 4. There is a correlation between the extent of the Somogyi effect and the growth hormone response to insulin, using a simple derived index to represent each function (P < 0·05). 5. Insulin secretion in normal subjects tends to be higher on the test than the control day, making inhibition of insulin release an unlikely primary mechanism. 6. The presence or absence of a Somogyi effect could not be related to insulin-induced changes in plasma Cortisol values. 7. Examination of individual cases supports the view that, while growth hormone may be mainly reponsible for the Somogyi effect, yet it is sometimes difficult to explain the effect without invoking other endocrine mechanisms.


1981 ◽  
Vol 138 (1) ◽  
pp. 51-55 ◽  
Author(s):  
S. A. Checkley ◽  
A. P. Slade ◽  
E. Shur

SummaryThe growth hormone response to clonidine was significantly less in 10 drug-free patients with endogenous depression than in 10 normal subjects who were individually matched with the patients for age and sex. The hypotensive and sedative effects of clonidine in the two groups were similar. The findings may indicate a defect at central a adrenoceptors at least in neuroendocrine systems.


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