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

Plasma vasopressin and atrial natriuretic hormone levels in hypopituitarism with and without hydrocortisone treatments: responses to an acute water load

1992 ◽  
Vol 126 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
Kazutoshi Sato ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Water Load ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic Hormone ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Atrial Natriuretic

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism. an acute oral water load of 20 ml·kg−1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N= 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.

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.

Water Intoxication in Normal Infants: Role of Antidiuretic Hormone in Pathogenesis

PEDIATRICS ◽  
1981 ◽  
Vol 68 (3) ◽  
pp. 349-353
Author(s):  
Ronald David ◽  
Demetrius Ellis ◽  
J. Carlton Gartner
Keyword(s):  
Clinical Improvement ◽  
Antidiuretic Hormone ◽  
Arginine Vasopressin ◽  
Therapeutic Intervention ◽  
Water Intoxication ◽  
Fluid Restriction ◽  
Urinary Osmolality ◽  
Symptom Complex ◽  
Plasma Arginine

Eight infants, 2 to 5 months of age, who were seen with somnolence or irritability, seizures, and hypothermia are described. The symptoms developed following the ingestion of dilute formula. All infants were hyponatremic. Three patients were identified by the symptom complex and were evaluated prior to any therapeutic intervention. Plasma arginine vasopressin concentration and urinary osmolality were either normal or increased despite hyponatremia and decreased serum osmolality. These data, coupled with rapid biochemical and clinical improvement following fluid restriction and/or administration of 3% NaCl, strongly implicate the excessive release of arginine vasopressin in the pathogenesis of this syndrome of water intoxication.

Effect of α-adrenergic blockade on pituitary hormonal responses to insulin-induced hypoglycemia in humans

1991 ◽  
Vol 125 (4) ◽  
pp. 372-377 ◽  
Author(s):  
B. Miles Fisher ◽  
Steve Thornton ◽  
David A. Hepburn ◽  
James J. Morton ◽  
Peter H. Baylis ◽  
...  
Keyword(s):  
Analysis Of Variance ◽  
Arginine Vasopressin ◽  
Maximum Plasma ◽  
Adrenergic Blockade ◽  
Hormonal Responses ◽  
Acute Hypoglycemia ◽  
Plasma Arginine ◽  
Control Plasma ◽  
Control Study

Abstract. Arginine vasopressin, oxytocin and ACTH are released from the pituitary gland in response to acute hypoglycemia. To investigate the role of α-adrenergic mechanisms in mediating this response, 6 non-diabetic subjects were studied during hypoglycemia induced by 0.15 IU/kg iv insulin under control conditions, and during non-selective α-adrenergic blockade with phentolamine. In the control study plasma arginine vasopressin rose from 1.6±0.8 pmol/l (mean ± sem) basally to a maximum of 2.5±0.8 pmol/l following hypoglycemia (p<0.05). An exaggerated response was found during phentolamine blockade, with a maximum plasma vasopressin of 11.5±0.4 pmol/l (by analysis of variance, p<0.05). The plasma oxytocin response to hypoglycemia was similarily increased during phentolamine compared to control. Plasma growth hormone rose to 94±19 mU/l, and during blockade with phentolamine the response was significantly reduced reaching a peak of 34±7 mU/l (by analysis of variance, p<0.05). ACTH and prolactin both increased in response to hypoglycemia, but the increases were not affected by phentolamine. An α-adrenergic mechanism appears to inhibit the release of arginine vasopressin and oxytocin in response to hypoglycemia, but does not appear to affect the secretion of ACTH.

Vasopressin and Malignant Deoxycorticosterone Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 45s-48s ◽  
Author(s):  
J. Möhring ◽  
B. Möhring ◽  
M. Petri ◽  
D. Haack
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Renal Hypertension ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Volume Depletion ◽  
Angiotensin System ◽  
Plasma Arginine ◽  
Normotensive Control

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin—angiotensin system plays in the pathogenesis of malignant renal hypertension.

Possible vascular role of increased plasma arginine vasopressin in congestive heart failure

2006 ◽  
Vol 106 (2) ◽  
pp. 191-195 ◽  
Author(s):  
Tomohiro Nakamura ◽  
Hiroshi Funayama ◽  
Akio Yoshimura ◽  
Yoshio Tsuruya ◽  
Muneyasu Saito ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Arginine Vasopressin ◽  
Plasma Arginine

Impaired Water Excretion in a Hyponatremic Patient following Thyroidectomy: Causal Role of Glucocorticoid Deficiency

1998 ◽  
Vol 24 (5) ◽  
pp. 341-347
Author(s):  
Katsuhiko Yonemura ◽  
Ryuichi Furuya ◽  
Yutaka Oki ◽  
Hideki Matsushima ◽  
Kazuhisa Ohishi ◽  
...  
Keyword(s):  
Causal Role ◽  
Water Excretion ◽  
Glucocorticoid Deficiency ◽  
Impaired Water

scholarly journals Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Katsunobu Yoshioka ◽  
Nagaaki Tanaka ◽  
Keiko Yamagami ◽  
Takeshi Inoue ◽  
Masayuki Hosoi
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
Human Study ◽  
Urine Osmolality ◽  
Water Excretion ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Saline Test

A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.5–4.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels during the hypertonic saline test. In conclusion, we showed in human study that masked diabetes insipidus could be mediated by AVP-independent mechanisms.

Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension

1977 ◽  
Vol 232 (3) ◽  
pp. F260-F269 ◽  
Author(s):  
J. Mohring ◽  
B. Mohring ◽  
M. Petri ◽  
D. Haack
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Biologically Active ◽  
Hypertensive Rats ◽  
Marked Enhancement ◽  
Plasma Arginine ◽  
The Relationship

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

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