Effect of angiotensin II on plasma ACTH in patients with Addison's disease

1985 ◽  
Vol 110 (4) ◽  
pp. 451-455
Author(s):  
Hermann Haller ◽  
Volker Bähr ◽  
Petra Exner ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Time Lag ◽  
Addison’S Disease ◽  
Major Effect ◽  
Addison's Disease ◽  
Base Line ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Short Term ◽  
Sodium Deficiency

Abstract. Short-term angiotensin II (All) infusions (3 ng/kg/min) were performed in 5 patients with Addison's disease in order to assess the effect of AII on ACTH secretion. Base line ACTH levels were elevated due to a 9-h time lag between hydrocortisone administration and onset of the study. In 2 separate infusion periods of 30-min duration, All had no unidirectional effect on plasma ACTH. Mean ACTH increased slightly but insignificantly. Mean blood pressure rose by about 10 mmHg. The degree of angiotensinaemia induced is probably similar to the state of moderate to severe sodium deficiency. Short-term changes of All in this order of magnitude have obviously no major effect on ACTH secretion.

No inhibition of corticotrophin (ACTH)-hypersecretion in adrenal insufficiency by somatostatin

1980 ◽  
Vol 95 (1) ◽  
pp. 71-74 ◽  
Author(s):  
A. Jara-Albarrán ◽  
J. Bayort ◽  
A. Caballero ◽  
R. Eusebio ◽  
P. García-Peris ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Primary Adrenal Insufficiency ◽  
No Inhibition ◽  
Infusion Period

Abstract. Somatostatin (250 μg as a bolus iv and 250 μg as a I h infusion) was administered to 6 patients with primary adrenal insufficiency (Addison's disease). The fall in plasma ACTH during the infusion period ranged between 0–30% with a mean reduction of 11.2 ± 11.6%. These findings suggest that with the method employed, somatostatin is not an inhibitor of ACTH secretion in a condition in which glucocorticoids are lacking.

Effects of fludrocortisone withdrawal on plasma angiotensin II, ACTH, vasopressin, and potassium in patients with Addison's disease

1987 ◽  
Vol 115 (3) ◽  
pp. 325-330 ◽  
Author(s):  
W. Oelkers ◽  
V. Bähr
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Feedback Inhibition ◽  
Addison’S Disease ◽  
Plasma Potassium ◽  
Dietary Sodium ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Plasma Angiotensin ◽  
Acth Release

Abstract. We attempted to answer to the question whether excessive rises in endogenous plasma angiotensin II (All) stimulate ACTH secretion by measuring PRA, All, AVP, ACTH, and cortisol in 8 patients with Addison's disease before and after withdrawal of fludrocortisone substitution. Blood was drawn at 14.30 h, exactly 6½ h after the morning dose of hydrocortisone had been taken. PRA and All were initially higher than normal in 4 patients. After withdrawal of fludrocortisone for 1 or 2 weeks, PRA and All rose markedly in 4 patients (up to 260 ng/l) without concomitant changes in plasma ACTH levels (r = −0.081, All vs ACTH). Changes in plasma cortisol could not have obscured a stimulatory effect of All on ACTH by variable feedback inhibition of ACTH release. The increase in plasma All levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. In all patients, hyperkalaemia developed after fludrocortisone withdrawal, independent of changes in PRA and AII. Rises in PRA, All, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Plasma AVP remained in the normal range after fludrocortisone withdrawal, but was slightly elevated after increasing salt intake without fludrocortisone administration. Conclusions: 1) Rises of endogenous plasma All to levels tenfold higher than normal do not stimulate ACTH release. All is probably not a physiological modulator of ACTH secretion. 2) Mineralocorticoid substitution in Addison's disease should be monitored by plasma potassium measurement. Hyperkalaemia may coexist with normal PRA.

Short-term angiotensin II infusion does not alter plasma ACTH in man

1984 ◽  
Vol 104 (4_Supplb) ◽  
pp. S113-S114
Author(s):  
H. HALLER ◽  
P. EXNER ◽  
V. BÄHR ◽  
W. OELKERS
Keyword(s):  
Angiotensin Ii ◽  
Plasma Acth ◽  
Short Term

Suppression of ACTH Secretion by Synthetic MSH-Release Inhibiting Factor PRO-LEU-GLY-NH2in Addison's Disease

1977 ◽  
Vol 9 (02) ◽  
pp. 150-152 ◽  
Author(s):  
K. Voigt ◽  
H. Fehm ◽  
R. Lang ◽  
K. Beinert ◽  
E. Pfeiffer
Keyword(s):  
Addison’S Disease ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Inhibiting Factor

Inhibitory effect of cyproheptadine on ACTH secretion in patients with Addison's disease

1983 ◽  
Vol 102 (1) ◽  
pp. 111-115
Author(s):  
P. Loli ◽  
F. Frascatani ◽  
D. Gelli ◽  
M. Maggioni ◽  
F. Muratori ◽  
...  
Keyword(s):  
Oral Dose ◽  
Single Oral Dose ◽  
Drug Administration ◽  
Plasma Levels ◽  
Addison’S Disease ◽  
Inhibitory Effect ◽  
Feedback Mechanism ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Acth Release

Abstract. In 14 patients with Addison's disease plasma levels of ACTH were studied after administration of a single oral dose (16 mg) of cyproheptadine. The drug administration was followed by an inhibition of ACTH release. These results support the view that cyproheptadine may exert an inhibitory effect on ACTH secretion in subjects whose corticosteroid feedback mechanism is normal. We hypothesize that the effect of cyproheptadine might be related to its anti-serotonin or anti-histaminergic action.

scholarly journals Effect of a pre-exercise hydrocortisone dose on short-term physical performance in female patients with primary adrenal failure

2016 ◽  
Vol 174 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Katerina Simunkova ◽  
Nevena Jovanovic ◽  
Espen Rostrup ◽  
Paal Methlie ◽  
Marianne Øksnes ◽  
...  
Keyword(s):  
Physical Activity ◽  
Aerobic Capacity ◽  
Healthy Subjects ◽  
Addison’S Disease ◽  
Exercise Stress ◽  
Addison's Disease ◽  
Short Term ◽  
Maximal Aerobic Capacity ◽  
Post Exercise ◽  
Stress Dose

ObjectiveMany patients with primary adrenal insufficiency (Addison's disease) take extra doses of glucocorticoids during stressful events, but a benefit has not been demonstrated in controlled trials. Here, we investigated the effects of a pre-exercise hydrocortisone dose on cardiorespiratory, hormonal and metabolic parameters in response to short-term strenuous physical activity.DesignThis was a randomized placebo-controlled, cross-over clinical trial.ParticipantsTen women with Addison's disease and 10 age-matched healthy females participated in the study.MeasurementsAll women in the study underwent maximal incremental exercise testing. A stress dose of 10 mg hydrocortisone or placebo was given 1 h prior to exercise on two occasions. Blood samples were drawn before, and 0, 15 and 30 min post exercise. Oxygen uptake, maximal aerobic capacity, endocrine and metabolic responses to physical activity, as well as health status by questionnaires were evaluated.ResultsMaximal aerobic capacity and duration of exercise were significantly lower in patients than in healthy subjects and did not improve with the treatment. After an extra hydrocortisone dose serum cortisol was significantly higher than in the healthy subjects (P<0.001). Post-exercise glucose and adrenaline levels were significantly lower and free fatty acids insignificantly higher in patients irrespective of stress dose. Stress dosing did not alter other metabolic or hormonal parameters or quality of life after the exercise.ConclusionsThe patients did not benefit from an extra dose of hydrocortisone in short strenuous exercise. Stress dosing may not be justified in this setting. Whether stress dosing is beneficial in other types of physical activity will have to be examined further.

Sign in / Sign up

Export Citation Format

Share Document