scholarly journals Role of antidiuretic hormone in the abnormal water diuresis of anterior hypopituitarism in man

1971 ◽  
Vol 50 (7) ◽  
pp. 1478-1489 ◽  
Author(s):  
Zalman S. Agus ◽  
Martin Goldberg
Keyword(s):  
Antidiuretic Hormone ◽  
Water Diuresis

The role of antidiuretic hormone in cold‐induced diuresis in the anaesthetized rat

1998 ◽  
Vol 162 (4) ◽  
pp. 475-480 ◽  
Author(s):  
BROMAN ◽  
KÄLLSKOG ◽  
NYGREN ◽  
WOLGAST
Keyword(s):  
Antidiuretic Hormone ◽  
Anaesthetized Rat

Effects of vasopressin administration on diuresis of water immersion in normal humans

1981 ◽  
Vol 51 (6) ◽  
pp. 1384-1387 ◽  
Author(s):  
M. Epstein ◽  
A. G. DeNunzio ◽  
R. D. Loutzenhiser
Keyword(s):  
Antidiuretic Hormone ◽  
Flow Rate ◽  
Water Immersion ◽  
Normal Subjects ◽  
Urinary Flow Rate ◽  
Urinary Flow ◽  
Relative Role ◽  
Normal Humans

Although previous studies have demonstrated that water immersion to the neck (NI) results in a significant diuresis, the mechanisms are incompletely delineated. Because recent studies in our laboratory have demonstrated that NI is associated with a suppression of antidiuretic hormone (ADH), it is possible that such a suppression mediates the encountered diuresis. The present study was undertaken to assess more directly the relative role of ADH suppression by determining the effects of vasopressin administration. Six hydrated normal subjects were studied on two occasions while undergoing 6 h of NI. During the second NI study, aqueous vasopressin (20 mU/h) was infused for the initial 4 h of study (NI + vasopressin). NI resulted in a significant increase in urinary flow rate beginning during hour 1 and persisting throughout NI. In contrast, during NI + vasopressin, the anticipated diuresis was abolished throughout the 4 h of vasopressin administration. Cessation of vasopressin administration during the final 2 h of NI + vasopressin resulted in a marked and prompt diuresis. The present observations are consistent with the formulation that ADH suppression participates importantly in mediating the diuresis of NI in hydrated normal subjects.

Vascular volume and blood level of antidiuretic hormone

1962 ◽  
Vol 202 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Leonard Share
Keyword(s):  
Antidiuretic Hormone ◽  
Blood Level ◽  
Peritoneal Lavage ◽  
Extracellular Fluid ◽  
Hypertonic Solution ◽  
Vascular Volume ◽  
Fourfold Increase ◽  
Chemical Procedure ◽  
Dextran Solution

The role of vascular volume in regulation of the blood level of antidiuretic hormone (ADH) was investigated utilizing a chemical procedure for extraction, isolation, and concentration of ADH in blood. The antidiuretic material recovered from blood was identified as ADH on the basis of its biological activity and the results of a number of chemical tests. Reduction in extracellular fluid volume by peritoneal lavage with hypertonic solution produced a fourfold increase in the blood titer of ADH within 20 min. Expansion of vascular volume at that time by the intravenous infusion of isotonic dextran solution resulted in a 50% reduction in the blood level of ADH. This reduction was maintained for the 30-min period of observation, although the blood level of ADH rose progressively when the lavage procedure was uninterrupted by infusion of dextran solution. It is concluded that blood volume is an important factor in regulation of blood concentration of ADH.

Autoradiographic analysis and regulation of angiotensin receptor subtypes AT4, AT1, and AT(1—7) in the kidney

2001 ◽  
Vol 281 (5) ◽  
pp. F936-F947 ◽  
Author(s):  
Rajash K. Handa ◽  
Shelly E. Handa ◽  
Monica K. S. Elgemark
Keyword(s):  
Cell Types ◽  
Receptor Subtypes ◽  
Receptor Density ◽  
Angiotensin Receptor ◽  
Puromycin Aminonucleoside ◽  
Water Diuresis ◽  
Receptor System ◽  
Numerous Cell ◽  
Autoradiographic Analysis

Receptor autoradiography revealed that angiotensin AT4 receptors were abundantly expressed in normal mammalian (mouse, rat, gerbil, guinea pig, rabbit) and avian (sparrow, chicken, turkey) kidneys and were more extensively distributed than previously reported (including proximal and distal segments of the nephron, interstitium, renal artery, vein, and ureter). Angiotensin AT4 receptors were generally found to be more abundant than angiotensin AT1 receptors in mammalian kidneys, whereas angiotensin AT(1—7) receptors were not detected in either mammalian or avian kidneys. Rats subjected to various chronic treatments were found to preferentially decrease kidney AT4 receptor density (furosemide, puromycin aminonucleoside, nitro-l-arginine methyl ester), decrease kidney AT1 receptor density (bilateral ureteral obstruction), or increase kidney AT1 receptor distribution in the inner medulla (water diuresis). These results indicate that the AT4 receptor can be expressed in numerous cell types within the normal kidney of several species. Furthermore, several models of renal dysfunction and injury have been identified that selectively alter kidney AT4 density and may potentially aid in elucidating the role of this novel angiotensin receptor system in renal function.

EFFECTS OF DEOXYCORTICOSTERONE ACETATE AND CORTISONE ON THE EXCRETION OF HYPOTONIC SALINE BY ADRENALECTOMIZED RATS

1954 ◽  
Vol 11 (3) ◽  
pp. 261-268 ◽  
Author(s):  
D. F. COLE
Keyword(s):  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
The Body ◽  
Renal Tubules ◽  
Water Diuresis ◽  
Deoxycorticosterone Acetate ◽  
Water Excretion ◽  
Normal Water ◽  
Hypotonic Saline ◽  
Adrenalectomized Rats

SUMMARY The response to loads of hypotonic saline has been investigated in intact and in adrenalectomized rats treated with deoxycorticosterone acetate, with cortisone acetate and with both steroids. The response of untreated adrenalectomized animals was also studied. Intact rats excreted more water than sodium during the 5 hr after loading with hypotonic saline. There was a reduction of the proportion of water reabsorbed in the renal tubules, but the proportion of sodium reabsorbed was unaltered. Adrenalectomized rats, either with or without deoxycorticosterone treatment, did not show this diuretic response, and there was evidence that sodium was lost from the body cells. Rats in these two groups reabsorbed a smaller proportion of sodium in their renal tubules than intactrats. Adrenalectomized rats treated with cortisone showed partial restoration of the ability to excrete water, but the renal loss of sodium was greater than in intact animals. Treatment of adrenalectomized rats with both cortisone and deoxycorticosterone restored water excretion to normal values, but excessive amounts of sodium were lost. In neither group which received cortisone was there any indication of loss of cell sodium. The response of rats in the group receiving both steroids was not a normal water diuresis because the animals were unable to excrete water without loss of sodium. It appeared unlikely that there was excessive antidiuretic hormone activity in the rats receiving cortisone and that some factor other than reduction of pituitary antidiuretic hormone secretion was essential for normal water diuresis.

Role of Antidiuretic Hormone in Impaired Urinary Dilution Associated with Chronic Bile-Duct Ligation

1980 ◽  
Vol 58 (6) ◽  
pp. 493-500 ◽  
Author(s):  
O. S. Better ◽  
G. A. Aisenbrey ◽  
T. Berl ◽  
R. J. Anderson ◽  
W. A. Handelman ◽  
...  
Keyword(s):  
Bile Duct ◽  
Antidiuretic Hormone ◽  
Bile Duct Ligation ◽  
Diluting Segment ◽  
Water Excretion ◽  
Duct Ligation ◽  
Normal Mean ◽  
And Function ◽  
Distal Delivery

1. The effect of chronic bile-duct ligation on systemic and renal haemodynamics and on the capacity to dilute the urine was studied in conscious rats. Sham-operated rats served as controls. 2. In the rats with bile-duct ligation, the maximal urinary diluting capacity was impaired, despite an expanded plasma volume, a normal mean arterial pressure and cardiac output, and normal intrarenal determinants of water excretion including distal delivery of fluid and function of the diluting segment. 3. In contrast, maximal urinary dilution capacity was intact in rats with congenital central diabetes insipidus and chronic bile-duct ligation. 4. It is concluded that the defect in urinary dilution in rats with chronic bile-duct ligation is dependent on antidiuretic hormone.

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