scholarly journals RESPONSES OF NORMAL SUBJECTS AND OF PATIENTS WITH DIABETES INSIPIDUS TO WATER AND SALT INGESTION 1

1939 ◽  
Vol 18 (4) ◽  
pp. 377-383 ◽  
Author(s):  
H. L. White ◽  
Thomas Findley
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.


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).


1988 ◽  
Vol 59 (02) ◽  
pp. 269-272 ◽  
Author(s):  
M B Grant ◽  
C Guay ◽  
R Lottenberg

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.


1993 ◽  
Vol 265 (6) ◽  
pp. R1247-R1252 ◽  
Author(s):  
A. M. Moses ◽  
B. Clayton

The secretion of arginine vasopressin (AVP) from the posterior pituitary is primarily and finely regulated by the osmolality of plasma. Even though a number of factors alter osmolality-induced release of AVP, there are no published data in humans that have addressed the role of chronic overhydration on this phenomenon. To address this problem we have identified eight patients with primary polydipsia using criteria not involving measurement of AVP, and have subjected them to standardized infusions of hypertonic saline. These patients had less AVP in both plasma and urine in relation to plasma osmolality than was found in normal subjects. In addition, their rate of rise of plasma and urine AVP was less than in normal subjects. Their osmotic threshold for AVP release may have been higher than normal. These data demonstrate that chronic overhydration in humans downregulates the release of AVP in response to hypertonicity. This phenomenon may explain the impairment of urine concentration in patients with primary polydipsia and emphasizes the basis of the difficulty that may occur clinically in differentiating between patients with primary polydipsia and partial central diabetes insipidus.


1988 ◽  
Vol 27 (7) ◽  
pp. 330-332 ◽  
Author(s):  
Eileen Doherty-Fuller ◽  
Kenneth C. Copeland

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