Growth Hormone and other Responses to Clonidine in Patients with Endogenous Depression

1981 ◽  
Vol 138 (1) ◽  
pp. 51-55 ◽  
Author(s):  
S. A. Checkley ◽  
A. P. Slade ◽  
E. Shur
Keyword(s):  
Growth Hormone ◽  
Normal Subjects ◽  
Endogenous Depression ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Sedative Effects ◽  
Drug Free ◽  
Age And Sex ◽  
Neuroendocrine Systems

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.

Growth Hormone Response to Clonidine After Recovery in Patients with Endogenous Depression

1988 ◽  
Vol 152 (1) ◽  
pp. 34-38 ◽  
Author(s):  
P. B. Mitchell ◽  
J. A. Bearn ◽  
T. H. Corn ◽  
S. A. Checkley
Keyword(s):  
Growth Hormone ◽  
Hypotensive Effect ◽  
Endogenous Depression ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Clinical Recovery ◽  
Trait Marker ◽  
Alpha2 Adrenoceptor ◽  
Drug Free

The growth hormone response to clonidine was measured in ten drug-free recovered patients, seven of whom had previously been tested when endogenously depressed, and compared with the response in ten individually matched controls. In eight of the patients there was an impairment of the growth hormone response, despite clinical recovery, although the hypotensive effect of clonidine in these patients was normal. This is suggestive of a persisting abnormal alpha2-adrenoceptor function in forebrain regions after recovery from an episode of endogenous depression, and may represent a trait marker for this condition.

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
Keyword(s):  
Growth Hormone ◽  
Time Course ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Acute Effects ◽  
Down Regulation ◽  
Adaptive Changes ◽  
Stopping Treatment ◽  
Rebound Increase

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.

The GH response to clonidine in endogenous as compared with reactive depression

1984 ◽  
Vol 14 (4) ◽  
pp. 773-777 ◽  
Author(s):  
S. A. Checkley ◽  
I. B. Glass ◽  
C. Thompson ◽  
T. Corn ◽  
P. Robinson
Keyword(s):  
Growth Hormone ◽  
Paired Comparison ◽  
Endogenous Depression ◽  
Reactive Depression ◽  
Age And Sex ◽  
Neuroendocrine Systems

SynopsisThe growth hormone (GH) response to clonidine was measured in 10 patients meeting standardized criteria for ‘endogenous’ depression and in 10 patients individually matched for age and sex but meeting the corresponding criteria for ‘reactive’ depression. In a paired comparison of patients with reactive and endogenous depression (matched for age and sex), the GH response to clonidine was less in the endogenous member of the pair in 8 out of 10 cases. These findings are interpreted as evidence of a defect at alpha2 adrenoceptors in neuroendocrine systems in endogenous as compared with reactive depression.

A Comparison of the Growth Hormone Responses to Clonidine and Apomorphine in the Same Patients with Endogenous Depression

1984 ◽  
Vol 144 (6) ◽  
pp. 636-639 ◽  
Author(s):  
T. H. Corn ◽  
A. S. Hale ◽  
C. Thompson ◽  
P. K. Bridges ◽  
S. A. Checkley
Keyword(s):  
Growth Hormone ◽  
Normal Subjects ◽  
Endogenous Depression ◽  
Hormone Responses ◽  
Dopaminergic Regulation ◽  
Similar Growth ◽  
Regulation Of Growth ◽  
Drug Free

SummaryThe growth hormone responses to clonidine (1.3 μg/kgm) and apomorphine (0.005 mg/kgm) have been measured in 8 drug free patients with endogenous depression. In these patients the growth hormone responses to clonidine were significantly smaller than to apomorphine. As these doses of clonidine and apomorphine have previously been reported to cause similar growth hormone responses in normal subjects, these findings support the hypothesis of a defect in the adrenergic but not the dopaminergic regulation of growth hormone in patients with endogenous depression.

The Effect of Hypoglycaemia on Oral Glucose Tolerance in Normal Subjects and Patients with Pituitary and Adrenal Disorders

1970 ◽  
Vol 39 (5) ◽  
pp. 663-674 ◽  
Author(s):  
N. W. Oakley ◽  
H. S. Jacobs ◽  
R. C. Turner ◽  
J. Williams ◽  
C. Dos ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Glucose Tolerance ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Saline Control ◽  
Oral Glucose ◽  
Hormone Response ◽  
Oral Glucose Tolerance ◽  
Brittle Diabetes ◽  
Insulin Test

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.

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