Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Depressed Patients

1985 ◽  
Vol 41 (2) ◽  
pp. 156-162 ◽  
Author(s):  
Fuad Lechin ◽  
Bertha van der Dijs ◽  
Daniela Jakubowicz ◽  
Rheyna E. Camero ◽  
Simon Villa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Plasma Levels ◽  
Depressed Patients

A Pilot Study of the Mechanism of Action of Desipramine

1981 ◽  
Vol 138 (3) ◽  
pp. 248-251 ◽  
Author(s):  
S. A. Checkley ◽  
A. P. Slade ◽  
E. Shur ◽  
S. Dawling
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Pilot Study ◽  
Mechanism Of Action ◽  
Depressed Patients ◽  
Sedative Effects ◽  
Before And After ◽  
Hormone Responses

SummaryTo test the hypothesis that desipramine alters α adrenoceptor function in depressed patients, the effects of clonidine upon growth hormone sedation and blood pressure have been measured in depressed patients before and after treatment with desipramine. After three weeks of treatment the hypotensive and sedative effects of clonidine were inhibited in all patients even though plasma desipramine concentrations at this time varied from 42 to 560 μg/l. Growth hormone responses to clonidine were enhanced in five of the six patients but this effect was not statistically significant. These findings are consistent with the hypothesis that in these patients desipramine altered α adrenoceptor function: other explanations are discussed.

Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Subjects

1985 ◽  
Vol 40 (3) ◽  
pp. 253-261 ◽  
Author(s):  
Fuad Lechin ◽  
Bertha van der Dijs ◽  
Daniela Jakubowicz ◽  
Rheyna Camero ◽  
Simón Villa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Plasma Levels

Downregulation of growth hormone in postural orthostatic tachycardia syndrome: insights from the SYSTEMA cohort

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Johansson ◽  
J Schulte ◽  
F Ricci ◽  
M Persson ◽  
R Sutton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Growth Hormone ◽  
Plasma Levels ◽  
Orthostatic Intolerance ◽  
Statistical Tests ◽  
Growth Hormone Level ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Funding Source ◽  
Significant Difference

Abstract Background Postural orthostatic tachycardia syndrome (POTS) is a variant of cardiovascular autonomic disorder occurring predominantly in young women. POTS is characterized by an excessive heart rate increase when assuming upright posture accompanied by symptoms of orthostatic intolerance. The pathophysiology of POTS has not been fully established and is believed to be multifactorial. Purpose We aimed to investigate the alterations in circulating growth hormone level in POTS. Methods We conducted an age-matched case-control study enrolling 42 patients with POTS (age 31±9 years; 36 women) verified by positive head-up tilt testing and cardiovascular autonomic tests, and 46 controls (32±9 years; 35 women) with negative active standing test and no history of syncope, orthostatic intolerance and endocrine disease. We measured plasma levels of growth hormone using a high-sensitivity chemiluminescence immunoassay in relation to presence of POTS diagnosis. All study participants completed the validated Orthostatic Hypotension Questionnaire (OHQ), consisting of two components: the symptoms assessment scale (OHSA) and daily activity scale (OHDAS) to evaluate the burden of symptoms. We applied standard statistical tests for group differences. Growth hormone values were log-transformed and standardized before the group comparison. Results POTS patients had significantly lower plasma levels of growth hormone (ng/mL) (median=0.53, IQR, 0.10–2.83 vs. median=2.33, IQR, 0.26–7.2, p=0.04) than controls. Levels of growth hormone were reversely related to OHDAS (p=0.049) among POTS patients. Supine heart rate was significantly higher in POTS patients (69.0±11.1 beats/min vs. 63.3±10.8 beats/min, p=0.02), as well as diastolic blood pressure (72.9±9.1 mmHg vs. 69.0±8.5 mmHg, p=0.04). We observed no significant difference in supine systolic blood pressure (116.6±13.3 mmHg vs. 115.2±10.0 mmHg, p=0.60). POTS patients had a significantly higher composite OHQ score than controls (60.0±18.6 vs. 4.2±7.5, p<0.001), as well as OHSA (36.2±10.0 vs. 3.6±6.4, p<0.001) and OHDAS (23.8±9.7 vs. 0.6±1.3, p<0.001). Conclusion(s) Our study shows that patients with POTS have significantly reduced plasma levels of circulating growth hormone. Lower growth hormone levels among POTS patients are associated with increased impairment of daily life activities. Further studies are necessary to confirm our findings in the independent populations and explain the mechanisms behind this alteration. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Crafoord Foundation, Swedish Heart and Lung Foundation

Plasma levels of ß-endorphin, cortisol, prolactin and growth hormone in depressed patients

1988 ◽  
Vol 78 (2) ◽  
pp. 230-233 ◽  
Author(s):  
R. Galard ◽  
J. Gallart ◽  
J. M. Arguello ◽  
S. Schwartz ◽  
J. M. Castellanos ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Levels ◽  
Depressed Patients

Growth hormone and physiological responses to clonidine in depression

1993 ◽  
Vol 23 (1) ◽  
pp. 57-63 ◽  
Author(s):  
Cornelius L. E. Katona ◽  
David Healy ◽  
Eugene S. Paykel ◽  
Andreas E. Theodorou ◽  
Kevin M. Lawrence ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Physiological Responses ◽  
Antidepressant Drugs ◽  
Psychoactive Drugs ◽  
Depressed Patients ◽  
Drug Free

SynopsisClonidine (1·3 μg/kg) was administered to 62 control and 55 depressed patients free of psychoactive drugs for at least 7 days and fasted overnight. Growth hormone (GH), pulse, blood pressure and sedation were measured every 15 min for 1 h before and 2 h after clonidine infusion.GH response did not differ significantly between control and depressed subjects overall or when divided by sex. The systolic hypotensive and sedative responses were blunted in depressed subjects compared with controls; these effects appeared to be secondary to residual antidepressant drugs since the differences were only significant for those depressed subjects with short drug-free intervals.No differences between depressed subjects and controls were seen in diastolic hypotensive or bradycardic responses and no differences in GH, cardiovascular or sedative responses were found between endogenous and non-endogenous depressed subjects.

The Effect of Mianserin on Alpha-2 Adrenergic Receptor Function in Depressed Patients

1984 ◽  
Vol 144 (4) ◽  
pp. 407-416 ◽  
Author(s):  
Dennis S. Charney ◽  
George R. Heninger ◽  
David E. Sternberg
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Adrenergic Receptor ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Term Treatment ◽  
Receptor Function ◽  
Depressed Patients ◽  
Long Term Treatment

SummaryRecent clinical investigations have shown that long term treatment with the tricyclic antidepressants desipramine and amitriptyline reduces the sensitivity of the alpha-2 adrenergic autoreceptor. In order to determine whether the tetracyclic antidepressant mianserin also has this action, the effect of clonidine, an alpha-2 adrenergic receptor agonist, on plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenlethyleneglycol (MHPG), blood pressure, and patient-rated sedation were measured in fifteen depressed patients before and during mianserin treatment. Postsynaptic alpha-2 adrenergic receptor function was assessed by measuring the growth hormone response to clonidine before and during treatment. Mianserin had little or no effect on the ability of clonidine to lower plasma MHPG and blood pressure, and to increase sedation and growth hormone secretion. The findings of this investigation indicates that long term mianserin treatment does not produce significant subsensitivity of the alpha-2 adrenergic receptor and suggests that a reduction in alpha-2 adrenergic autoreceptor sensitivity is not a necessary action for all effective antidepressant treatments.

Alpha-2 Adrenergic Receptor Sensitivity and the Mechanism of Action of Antidepressant Therapy

1983 ◽  
Vol 142 (3) ◽  
pp. 265-275 ◽  
Author(s):  
Dennis S. Charney ◽  
George R. Heninger ◽  
David E. Sternberg
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Mechanism Of Action ◽  
Plasma Levels ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Receptor Sensitivity ◽  
Antidepressant Treatments ◽  
Plasma Mhpg ◽  
Adrenergic Receptor Agonist

SummaryIt has been hypothesized that the mechanism of action of antidepressant treatments is related to their ability to decrease the sensitivity of the alpha-2 adrenergic autoreceptor. In order to assess alpha-adrenergic autoreceptor sensitivity, the effects of clonidine, the alpha-2 adrenergic receptor agonist, on plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenethyleneglycol (MHPG), blood pressure (BP) and patient-rated sedation were measured in nine depressed patients before and during amitripytline treatment. Postsynaptic alpha-2 adrenergic receptor sensitivity was assessed by determining the growth hormone (GH) response to clonidine before and during treatment. Amitriptyline significantly attenuated the effects of clonidine on plasma MHPG, standing systolic BP, and sedation, indicating that alpha-2 adrenergic autoreceptors had become subsensitive. In addition, baseline plasma MHPG levels were significantly reduced. Amitriptyline had no effect on the GH response to clonidine.

The Involvement of Platelets and the Coronary Vasculature in Collagen-Induced Sudden Death in Rabbits

1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Platelet Count ◽  
Sudden Death ◽  
Myocardial Ischaemia ◽  
Plasma Levels ◽  
Sodium Citrate ◽  
Plasma Samples ◽  
Calcium Entry Blockers

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.

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