Role of Hypovolemia in the Impaired Water Diuresis of Adrenal Insufficiency1

1970 ◽  
Vol 30 (2) ◽  
pp. 252-258 ◽  
Author(s):  
GEORGE L. ACKERMAN ◽  
LINDSEY MILLER
Keyword(s):  
Water Diuresis ◽  
Impaired Water

scholarly journals Role of plasma arginine vasopressin in the impaired water diuresis of isolated glucocorticoid deficiency in the rat

1980 ◽  
Vol 17 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Ira N. Mandell ◽  
Ralph A. DeFronzo ◽  
Gary L. Robertson ◽  
John N. Forrest
Keyword(s):  
Arginine Vasopressin ◽  
Water Diuresis ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Impaired Water

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.

The role of vasopressin in the impaired water excretion of myxedema

1978 ◽  
Vol 64 (4) ◽  
pp. 613-621 ◽  
Author(s):  
W.Ronald Skowsky ◽  
Thomas A. Kikuchi
Keyword(s):  
Water Excretion ◽  
Impaired Water

Pathological Role of Aquaporin-2 in Impaired Water Excretion and Hyponatremia

2004 ◽  
Vol 16 (4) ◽  
pp. 293-296 ◽  
Author(s):  
S. Ishikawa ◽  
T. Saito ◽  
K. Kasono
Keyword(s):  
Water Excretion ◽  
Aquaporin 2 ◽  
Impaired Water

Effects of Glucocorticoid Deficiency on Renal Medullary Cyclic Adenosine Monophosphate of Rats

1978 ◽  
Vol 54 (5) ◽  
pp. 573-577 ◽  
Author(s):  
K. Kurokawa ◽  
E. Aznar ◽  
C. Descoeudres ◽  
Anicia Zulueta ◽  
S. G. Massry
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Antidiuretic Hormone ◽  
Adenosine Monophosphate ◽  
Water Diuresis ◽  
Glucocorticoid Deficiency ◽  
Impaired Water ◽  
Adrenalectomized Rats

1. The effects of adrenalectomy on the adenylate cyclase—adenosine 3′:5′-cyclic monophosphate (cyclic AMP) system of rat renal medulla were examined to evaluate the mechanism of the impaired water diuresis in glucocorticoid deficiency. 2. Concentrations of cyclic AMP in medullary tubules from adrenalectomized rats were significantly higher than in the tubules from control animals both in the presence and absence of antidiuretic hormone. 3. This abnormality was corrected by the treatment in vivo of the adrenalectomized rats with dexamethasone, but addition of this drug to the incubation medium did not abolish the differences in cyclic AMP between tubules from adrenalectomized and normal rats. 4. The activity of adenylate cyclase or cyclic AMP phosphodiesterase in vitro was not affected by adrenalectomy. 5. In glucocorticoid deficiency, the concentration of cyclic AMP in medullary tubules is increased both with and without antidiuretic hormone. This abnormality may render medullary tubules more permeable to water and may underlie the impaired water diuresis in glucocorticoid deficiency.

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