ANTIDIURETIC EFFECT OF AN ANTICONVULSANT DRUG (5-CARBAMYL-5H-DIBENZO(B,F)AZEPIN = TEGRETAL) ASSOCIATED WITH MEASURABLE INCREASE OF ADH ACTIVITY IN SERUM OF PATIENTS SUFFERING FROM DIABETES INSIPIDUS AND OF PATIENTS WITH POLYURIA AND POLYDIPSIA FOLLOWING HYPOPHYSECTOMY

1969 ◽  
Vol 61 (1_Suppl) ◽  
pp. S240 ◽  
Author(s):  
H. Frahm ◽  
E. Smejkal ◽  
R. Kratzenstein
2005 ◽  
Vol 5 (2) ◽  
pp. 38-42 ◽  
Author(s):  
Elvedina Kapić ◽  
Fahir Bečić ◽  
Maida Todić

In this paper we have reviewed the possition of desmopressin in the treatment of diabetes insipidus. Desmopressin is a synthetic analog of vasopressin, with more pronounced antidiuretic effect. It is treatment of choice in substitution therapy of diabetes insipidus. Its application before sleeping time can reduce nocturnal enuresis, so it has a place in the treatment of enuresis nocturna. Antidiuretic effect of desmopressin is the result of agonistic effect on V2 receptors in the renal tubules. The efficacy and safety of desmopressin in mentioned indications was confirmed in clinical studies.


1972 ◽  
Vol 68 (3_Suppl) ◽  
pp. S51 ◽  
Author(s):  
F. Uhlich ◽  
K. Loeschke ◽  
J. Eigler

Author(s):  
T.F. Lévêque

The history of the hypothalamus and neuroendocrinology is so intimately related to the development of our ideas on the disease known as diabetes insipidus, that any discussion of the one must include a discussion of the other. Many authors have compared the history of diabetes insipidus to a comedy of errors. Indeed, the whole problem seems to have fared rather badly from the very beginning when Magnus and Schafer (1901), and Schafer and Herring (1905) demonstrated that extracts of the posterior lobe of the pituitary body had a diuretic effect rather than the antidiuretic effect as we know it today. Furthermore, from a histological point of view, Herring (1908) and later Cushing (1933) were of the opinion that the cellular constituents of the posterior lobe were incapable of secreting the active factors attributed to that lobe and that consequently a search had to be made elsewhere for the secretory cells. Herring (1913) visualized the secreting cells as coming from the pars intermedia and migrating into the pars nervosa where they degenerated and released the “hormones”. Cushing (1933) fully subscribed to this and in 1933 stated rather emphatically that “it is scarcely conceivable that the neural core of the lobe is capable independently of elaborating a hormone.”


Pharmacology ◽  
1970 ◽  
Vol 3 (2) ◽  
pp. 122-128 ◽  
Author(s):  
J.P. Radó ◽  
L. Borbély ◽  
L. Szende ◽  
J. Takó

1990 ◽  
Vol 123 (6) ◽  
pp. 657-660 ◽  
Author(s):  
Mustafa Koçak ◽  
Bülent Mustafa Karademir ◽  
Tamer Tetiker

Abstract. Indapamide produced a significant decrease in urinary output in three patients with central diabetes insipidus. The 24-h urinary volume was reduced from 5 to 2.3 1 in a 39-year-old woman; from 11 to 4.3 1 in a 30-year-old man, and from 16 to 9.2 1 in a 40-year-old man receiving 2.5 mg of indapamide per day. To our knowledge, the antidiuretic effect of indapamide in central diabetes insipidus has not been reported previously.


1982 ◽  
Vol 63 (6) ◽  
pp. 525-532 ◽  
Author(s):  
S. J. Walter ◽  
J. Skinner ◽  
J. F. Laycock ◽  
D. G. Shirley

1. The antidiuretic effect of hydrochlorothiazide in diabetes insipidus was investigated in rats with the hereditary hypothalamic form of the disease (Brattleboro rats). 2. Administration of hydrochlorothiazide in the food resulted in a marked fall in urine volume and a corresponding rise in osmolality. These effects persisted throughout the period of treatment (6–7 days). 3. Body weight and extracellular volume were significantly reduced in the thiazide-treated rats. 4. Hydrochlorothiazide caused an increase in urinary sodium excretion only on the first day of treatment. The resulting small negative sodium balance (in comparison with untreated rats) remained statistically significant for 2 days only. Thiazide-treated rats gradually developed a potassium deficit which was statistically significant from the fourth day of treatment. 5. Total exchangeable sodium, measured after 7 days of thiazide treatment, was not significantly different from that of untreated rats. However, plasma sodium was reduced in thiazide-treated animals, whereas erythrocyte sodium concentration was elevated. 6. It is concluded that the antidiuresis resulting from chronic hydrochlorothiazide administration is associated with a reduction in extracellular volume, but not with a significant overall sodium deficit. Hydrochlorothiazide appears to cause a redistribution of the body's sodium such that the amount of sodium in the extracellular fluid compartment is reduced.


1961 ◽  
Vol 22 (1) ◽  
pp. 77-86 ◽  
Author(s):  
G. C. KENNEDY ◽  
J. D. CRAWFORD

SUMMARY Chlorothiazide and its analogues had a marked antidiuretic action in diabetes insipidus; the effect appeared to be independent of that of antidiuretic hormone. In a series of rats which had been treated with these saluretic drugs, subsequent adrenalectomy had a similar antidiuretic effect. Chlorothiazide produced little or no further antidiuresis in these adrenalectomized animals, but it prevented the restoration of polyuria which otherwise followed the administration of adrenal steroids. It is suggested that the distal part of the renal tubule where osmotically free water is released is a site of action common to chlorothiazide and corticoids.


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