Vasopressin-dependent upregulation of aquaporin-2 gene expression in glucocorticoid-deficient rats

Saitô, Takako; Ishikawa, San E.; Ando, Fumiko; Higashiyama, Minori; Nagasaka, Shoichiro; Sasaki, Sei; Saito, Toshikazu

doi:10.1152/ajprenal.2000.279.3.f502

Cited by 63 publications

(54 citation statements)

References 34 publications

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“…In experimental models of glucocorticoid deficiency non-suppressible release of AVP is found despite hypo-osmolality, which should suppress AVP release to undetectable levels (5 -7). We have demonstrated that the AVP V 2 receptor antagonist blocked the upregulation of AQP-2 mRNA expression and promptly normalized renal water excretion in glucocorticoid-deficient rats (12). Also, similar results were obtained with hydrocortisone replacement in glucocorticoid-deficient rats and patients with hypopituitarism, i.e.…”

Section: Discussionsupporting

confidence: 77%

“…Also, similar results were obtained with hydrocortisone replacement in glucocorticoid-deficient rats and patients with hypopituitarism, i.e. hydrocortisone replacement normalizes AVP secretion, urinary excretion of AQP-2 and water diuresis (4,6,9,10,12,22). Therefore, non-suppressible secretion of AVP plays a crucial role in impaired water excretion in secondary adrenal insufficiency.…”

Section: Discussionsupporting

confidence: 69%

“…Non-suppressible release of arginine vasopressin (AVP) was found despite hypo-osmolality which should suppress AVP release to undetectable levels (3,6,7,11). In addition, the expression of aquaporin-2 (AQP-2) water channel mRNA and protein in kidney was upregulated in glucocorticoid-deficient rats (12). Hydrocortisone replacement corrected the defect in renal water excretion and normalized plasma AVP levels and kidney AQP-2 mRNA expression in glucocorticoid deficiency (6,7,12).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the expression of aquaporin-2 (AQP-2) water channel mRNA and protein in kidney was upregulated in glucocorticoid-deficient rats (12). Hydrocortisone replacement corrected the defect in renal water excretion and normalized plasma AVP levels and kidney AQP-2 mRNA expression in glucocorticoid deficiency (6,7,12).…”

Section: Introductionmentioning

confidence: 99%

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Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

et al. 2003

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Objective: Hyponatremia occurs not infrequently in hypopituitarism. Arginine vasopressin (AVP)-induced impaired water excretion is found in patients with hypopituitarism and experimental models of glucocorticoid deficiency. Design: The present study was undertaken to determine whether augmented release of AVP is involved in the development of hyponatremia in elderly subjects with secondary adrenal insufficiency. Methods: Forty patients with ACTH-deficient, secondary adrenal insufficiency were examined. They were divided into three groups according to the age at which diagnosis was ascertained (group A , 20 years, group B 20-64 years, and group C $ 65 years). Results: Hyponatremia was more manifest in the elderly group than in the other two groups, serum sodium (Na) levels being 124.7 mmol/l in the elderly group, a value significantly less than 141.5 and 133.5 mmol/l in groups A and B. Plasma AVP levels seemed likely to be high compared with the respective hypo-osmolality in plasma in the elderly group, as plasma AVP levels were 1.7 pmol/l despite a mean plasma osmolality of 259 mmol/kg. Such an alteration was less clear in group B and was not found in group A. Therefore, elevation of plasma AVP was apparent in the elderly patients. Hydrocortisone replacement promptly normalized serum Na levels from 125 to 142 mmol/l ðP , 0:01Þ and reduced plasma AVP levels from 1.7 to 0.9 pmol/l ðP , 0:05Þ; which were comparable to the respective plasma osmolality in the elderly patients. Conclusion: These results indicate that non-suppressible release of AVP is crucially involved in the impaired water excretion and hyponatremia seen in elderly patients with secondary adrenal insufficiency compared with the younger patients, and that exaggerated release of AVP becomes manifest as the subjects grow older.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

et al. 2003

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“…Finally, peptide (7) and nonpeptide V 2 receptor antagonists (23) have been shown to dramatically enhance the renal capacity to excrete solute-free water in GD. Thus the nonosmotic release of AVP during GD may involve direct hypothalamic and peripheral baroreceptor pathways.The effect of GD on renal AQP2 expression is less clear (11,23). However, in a recent study, Saito et al (23) demonstrated an AVP-dependent increase in renal medullary AQP2 expression in GD rats.…”

mentioning

confidence: 99%

Molecular analysis of impaired urinary diluting capacity in glucocorticoid deficiency

Wang¹,

Li²,

Summer³

et al. 2006

American Journal of Physiology-Renal Physiology

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Urinary diluting ability and protein abundance of renal aquaporins (AQPs) and ion transporters in glucocorticoid-deficient (GD) rats were examined at baseline and in response to oral water loading. Rats underwent bilateral adrenalectomy followed by aldosterone (GD) or aldosterone ϩ dexamethasone (CTL) replacement. Before oral water loading, urinary output was significantly decreased and urinary osmolality (Uosm) was increased in GD compared with CTL rats. Protein abundance of inner medullary AQP2 (148 Ϯ 18%), phosphorylated AQP2 (pAQP2, 156 Ϯ 13%), and AQP3 (145 Ϯ 8%) was significantly upregulated in GD compared with CTL rats (all P Ͻ 0.05). GD rats also demonstrated a marked reduction in urinary Na ϩ excretion compared with pair-fed CTL rats. Na ϩ -K ϩ -2Cl Ϫ cotransporter, Na ϩ /H ϩ exchanger type 3, and cortical ␤-and ␥-subunits of the epithelial Na ϩ channel were significantly upregulated in GD rats. At 1 h after an acute water load (40 ml/kg by oral gavage), GD rats demonstrated a decrease in percent water excretion (5 Ϯ 1 vs. 33 Ϯ 9%, P Ͻ 0.01) and urinary output (33 Ϯ 12 vs. 250 Ϯ 65 l ⅐ kg Ϫ1 ⅐ min Ϫ1 , P Ͻ 0.05) and an increase in Uosm (1,894 Ϯ 292 vs. 316 Ϯ 92 mosmol/kgH2O, P Ͻ 0.001) compared with CTL rats. Plasma AVP was increased (1.6 Ϯ 0.2 vs. 0.9 Ϯ 0.2 pg/ml, P Ͻ 0.05), as was protein expression of inner medullary AQP2 (149 Ϯ 5%) and pAQP2 (177 Ϯ 9%, P Ͻ 0.01), in GD compared with CTL rats; apical expression of AQP2 was maintained in GD rats. The vasopressin V 2 receptor antagonist OPC-31260 increased percent water excretion and urinary output and reduced Uosm compared with vehicle-treated GD rats. OPC-31260 also reversed the increased abundance and apical trafficking of inner medullary AQP2 and pAQP2 protein in GD rats. In conclusion, enhanced protein abundance of Na ϩ transporters and Na ϩ channels with Na ϩ retention occurred with GD. OPC-31260 reversed upregulation and apical trafficking of AQP2 and pAQP2 in association with improved urinary diluting capacity and increased water excretion after oral water loading. arginine vasopressin; aquaporin; impaired urinary dilution THE PATHOGENESIS OF ALTERED salt and water metabolism in adrenal insufficiency is complex, with proposed mechanisms in mineralocorticoid deficiency that are quite different from those in glucocorticoid deficiency (GD). Thus these hormonal disorders must be selectively and independently investigated. Both conditions are associated with hyponatremia and impaired urinary dilution. Mineralocorticoid deficiency, however, is associated with urinary Na ϩ wasting, diminished extracellular fluid volume, nonosmotic release of arginine vasopressin (AVP) (7), and upregulation of the AVP-responsive aquaporin (AQP)-2 (AQP2) water channel in the renal collecting duct (18). It has been shown that maintenance of Na ϩ balance during mineralocorticoid deficiency abolishes water retention and hyponatremia (18), whereas administration of vasopressin V 2 receptor antagonists markedly improves, but does not totally correct, the associated impairmen...

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A case of extreme hyponatremia without neurologic symptoms

Zhou

Chen²

2019

Clinical Case Reports

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Vasopressin-dependent upregulation of aquaporin-2 gene expression in glucocorticoid-deficient rats

Cited by 63 publications

References 34 publications

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

Molecular analysis of impaired urinary diluting capacity in glucocorticoid deficiency

A case of extreme hyponatremia without neurologic symptoms

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