DER INSULINHYPOGLYKÄMIE-TEST ALS FUNKTIONSPRÜFUNG DES HYPOTHALAMUS-HYPOPHYSEN-NEBENNIERENRINDEN-SYSTEMS.

1967 ◽  
Vol 54 (4) ◽  
pp. 681-695 ◽  
Author(s):  
H. Bethge ◽  
K. Irmscher ◽  
H. G. Solbach ◽  
W. Winkelmann ◽  
H. Zimmermann ◽  
...  

ABSTRACT In 50 patients determinations of blood sugar and corticosteroids in plasma (11-OHCS) were carried out during insulin-induced hypoglycaemia. In 9 out of 11 patients with Cushing's syndrome (bilateral adrenal hyperplasia) the characteristic finding was a missing increase of 11-OHCS concentrations during hypoglycaemia. On the contrary, 5 patients with alimentary obesity and clinical signs of hypercorticism showed a normal or even increased adrenocortical response. The results obtained in 7 patients with uncomplicated central diabetes insipidus did not differ from those in normal subjects, while 2 further patients with diabetes insipidus, complicated with secondary adrenocortical insufficiency, failed to respond. Findings in 12 patients with anorexia nervosa are consistent with a normal function of the hypothalamo-pituitary-adrenal axis. According to plasma corticosteroid response during hypoglycaemia results obtained in 15 patients with disorders of hypothalamus and/or hypophysis may be divided into three groups. The significance of this classification with regard to replacement therapy is discussed. Observations show that plasma corticosteroid estimations during insulin-induced hypoglycaemia provide a simple and reliable method to ascertain the function of the hypothalamo-pituitary-adrenal axis (insulinhypoglycaemiatest).

1983 ◽  
Vol 29 (5) ◽  
pp. 882-884 ◽  
Author(s):  
J Camps ◽  
A Martínez-Vea ◽  
R M Pérez-Ayuso ◽  
V Arroyo ◽  
J M Gaya ◽  
...  

Abstract A radioimmunoassay for arginine-vasopressin in human plasma with use of a commercially available antibody was developed and evaluated. The hormone was extracted from plasma with cold 98% ethanol, which showed a significantly higher (p less than .001) and more precise recovery than with the acetone-ether procedure (65.3 +/- 3.7% vs 50.8 +/- 6.0%, respectively). The sensitivity was 0.31 pg per tube. Results for normal subjects in different physiological conditions and in patients with diabetes insipidus and inappropriate antidiuretic hormone secretion showed the good reliability of the method.


1970 ◽  
Vol 39 (4) ◽  
pp. 517-527 ◽  
Author(s):  
M. A. Barraclough ◽  
N. F. Jones

1. Changes in the urinary concentrations or urine/plasma (U/P) ratios of creatinine, urea, sodium and potassium were determined during the transition from water diuresis to antidiuresis when normal subjects and patients with diabetes insipidus were given injections of vasopressin. 2. In confirmation of previous work, it was found that after vasopressin administration the urinary concentration or U/P ratio of urea rose to a lesser degree than that of creatinine, indicating an increase in the tubular reabsorption of urea. 3. The urinary concentration, or U/P ratio, of sodium also rose to a lesser degree than that of creatinine. Thus vasopressin also increases the tubular reabsorption of sodium. 4. In contrast, the urinary concentration or U/P ratio of potassium tended to rise more than that of creatinine, indicating a decrease in the net tubular reabsorption of potassium. 5. Quantitative changes in the tubular handling of these urinary solutes were assessed by calculating the ratio—solute concentration during antidiuresis/solute concentration during diuresis—and then expressing this as a percentage of the corresponding ratio for creatinine. In subjects on a normal or high sodium intake the values thus obtained were: urea 72% (99% confidence limits 65–81%); sodium 79% (99% confidence limits 68–92%) and potassium 119% (99% confidence limits 102–139%). 6. In salt depleted subjects the values for these ratios were: urea 63% (99% confidence limits 60–65%) and sodium 36% (99% confidence limits 33–40%). Vasopressin had no consistent effect on potassium reabsorption in salt depleted subjects. 7. The effects of vasopressin on normal subjects and on patients with diabetes insipidus were similar. 8. It is suggested that these effects of vasopressin on sodium and potassium handling by the kidney occur in the collecting duct.


1984 ◽  
Vol 30 (2) ◽  
pp. 259-265 ◽  
Author(s):  
W E Nicholson ◽  
D R Davis ◽  
B J Sherrell ◽  
D N Orth

Abstract This RIA for corticotropin (ACTH) involves use of a commercially available antiserum and permits measurement of immunoreactive ACTH in unextracted plasma. The assay takes 2.5 days, detects as little as 5 pg/mL of plasma, and is specific: structurally and (or) biosynthetically related peptides do not cross react. Generally, data on dilutions of almost all human plasma specimens produce curves parallel to that for the ACTH reference standard. Values correlate well with those obtained by a well-established but more laborious RIA. We measured immunoreactive ACTH in normal subjects at various times of the day and after modulation of their pituitary-adrenal axis, and in patients with hypo- and hyper-secretion of ACTH. We conclude that the full range of immunoreactive ACTH values, which accurately reflect the status of the subject's pituitary-adrenal axis, can be quickly and easily determined in samples of unextracted human plasma.


1980 ◽  
Vol 58 (3) ◽  
pp. 193-200 ◽  
Author(s):  
T. Bennett ◽  
D. J. Hosking ◽  
J. R. Hampton

1. Cardiovascular responses to graded increments of lower body negative pressure were studied in non-diabetic subjects and in patients with diabetes mellitus. 2. In all subjects, low levels of negative pressure (which did not affect significantly systemic arterial pressure) induced forearm vasoconstriction, suggesting normal function of the ‘low pressure’ cardiopulmonary baroreflex. However, in some diabetic patients the response to higher levels of negative pressure was abnormal, and it seems likely that although afferent mechanisms were intact there was impairment of efferent vasoconstrictor function. 3. Changes in R—R interval were linearly related to changes in systolic blood pressure induced by higher levels of negative pressure. The slope of the relationship was taken as the sensitivity of the ‘high pressure’ arterial baroreflex; diabetic patients showed a reduced sensitivity compared with normal subjects. Furthermore, in diabetic patients, abnormalities of R—R interval control were more common than abnormalities of vasoconstrictor function, suggesting that heart-rate control is impaired earlier than vasomotor function in diabetic autonomic neuropathy.


1990 ◽  
Vol 122 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Søren Boesgaard ◽  
Claus Hagen ◽  
Anders Nyboe Andersen ◽  
Mogens Fenger ◽  
Ebbe Eldrup

Abstract. The regulation of the hypothalamic-pituitary-adrenal axis by dopamine is not fully understood. Therefore, we have studied the effect of dopamine, metoclopramide, a D-2 receptor antagonist, and fenoldopam, a specific D-1 receptor agonist, on ACTH and cortisol levels in normal subjects. Normal women received 5-h infusions of either glucose (N = 6) or dopamine at rates of 0.04 (N = 6), 0.4 (N = 6) and 4.0 μg · kg−1· min−1 (N = 8). After 3 h, 10 mg metoclopramide was given iv. No intergroup differences regarding ACTH and cortisol levels were observed (p>0.05). In a second study six women received dopamine (4.0 μg·kg−1·min−1) or glucose for 18 h. During the infusions cortisol and ACTH levels were similar on the two study days. Administration of metoclopramide (10 mg) after 17 h induced a significant increase in cortisol levels during dopamine infusion (p<0.05), whereas no effect was observed during placebo infusion. ACTH levels were unaffected by metoclopramide. In a third study, 9 normal women and 9 normal men received fenoldopam (0.5 μg·kg −1·min−) or placebo infusions for 3 h. In males, median ACTH and cortisol levels were significantly lower (p<0.05) during fenoldopam compared with placebo infusion. In contrast, fenoldopam did not affect ACTH and cortisol levels in normal women. The results suggest that the effect of dopamine D-1 receptor stimulation on ACTH and cortisol secretion is mainly at the hypothalamic level and that this effect is sex-dependent. In addition, we hypothesize that raised dopaminergic activity for a prolonged period of time may have an inhibitory effect on the hypothalamic-pituitary-adrenal axis. This may be triggered by low estrogen levels.


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