Plasma Arginine Vasopressin in diabetic ketoacidosis

Walsh, Caroline; Baylis, P. H.; Malins, J. M.

doi:10.1007/bf01225456

Cited by 46 publications

(23 citation statements)

References 13 publications

(12 reference statements)

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“…All subsequent studies in humans with either type I or type II (non-insulin-dependent) DM have confirmed this finding, although the magnitude of the elevation varies from one study to another [3, 4, 5, 6, 7]. In rats, streptozotocin-induced DM results in a 2- to 7-fold elevation in P VP [8, 9, 10, 11, 12], and rats with a genetic form of DM (BB rats) exhibit an even greater elevation [9].…”

Section: Vasopressin Elevation In Diabetes Mellitusmentioning

confidence: 58%

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Vasopressin and Diabetes mellitus

Bankir¹,

Bardoux²,

Ahloulay³

2001

Nephron

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In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the developement of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.

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Section: Vasopressin Elevation In Diabetes Mellitusmentioning

confidence: 58%

“…A correlation also exists between the DM-control difference in P VP and the corresponding difference in glycemia among the five studies (r = 0.680, p < 0.05). In humans as in rats, correction of ketoacidosis and/or hyperglycemia is accompanied by a significant reduction in P VP [3, 4, 7, 13] and thirst [5]. …”

Section: Vasopressin Elevation In Diabetes Mellitusmentioning

confidence: 99%

Vasopressin and Diabetes mellitus

Bankir¹,

Bardoux²,

Ahloulay³

2001

Nephron

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“…4d). AVP time course experiments were performed on WT CCDs for 80 min following an established baseline for 20 min, and confirmed that the AVP response is maintained at 50-70% above baseline (p < 0.05; n = 5) throughout the experimental period Urinary AVP excretion rate and medullary V2 receptor and urea transporter α1 expression AVP levels are elevated in diabetes despite the presence of polyuria and inability to adequately concentrate urine [1,[23][24][25][26][27]. Since we observed changes in AQP2, which is physiologically regulated by AVP, we measured urinary AVP excretion [17].…”

Section: Aqp1 and Aqp2 In Epmentioning

confidence: 67%

PGE2 receptor EP3 inhibits water reabsorption and contributes to polyuria and kidney injury in a streptozotocin-induced mouse model of diabetes

et al. 2016

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Aims/hypothesis The first clinical manifestation of diabetes is polyuria. The prostaglandin E 2 (PGE 2 ) receptor EP 3 antagonises arginine vasopressin (AVP)-mediated water reabsorption and its expression is increased in the diabetic kidney. The purpose of this work was to study the contribution of EP 3 to diabetic polyuria and renal injury. -STZ mice also had increased protein expression of aquaporin-1, aquaporin-2, and urea transporter A1, and reduced urinary AVP excretion, but increased medullary V2 receptors. In vitro microperfusion studies indicated that Ep 3 −/− and WT-STZ CDs responded to AVP stimulation similarly to those of wild-type mice, with a 60% increase in fluid reabsorption. In WT non-injected and WT-STZ mice, EP 3 activation with sulprostone (PGE 2 analogue) abrogated AVP-mediated water reabsorption; this effect was absent in mice lacking EP 3 . A major finding of this work is that Ep 3 −/− -STZ mice showed blunted renal cyclooxygenase-2 protein expression, reduced renal hypertrophy, reduced hyperfiltration and reduced albuminuria, as well as diminished tubular dilation and nuclear cysts. Conclusions/interpretation Taken together, the data suggest that EP 3 contributes to diabetic polyuria by inhibiting expression of aquaporins and that it promotes renal injury during diabetes. EP 3 may prove to be a promising target for more selective management of diabetic kidney disease.

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“…The plasma AVP level was increased in patients with insulindependent diabetes mellitus (IDDM) or non-IDDM (NIDDM) (14,15), and treating these subjects with insulin or sulfonylurea improved not only the plasma glucose level but also the plasma AVP level (16,17). In addition, the binding activity of AVP to the liver, in which the V1a receptors were predominantly expressed, decreased in the ob/ob mice and the streptozotocin-induced diabetes mellitus rat, whereas the binding activity to the kidney, in which the V2 receptors were predominantly expressed, was not altered (18,19).…”

Section: A Rginine-vasopressin (Avp) Is a Neuropeptidementioning

confidence: 99%

Alteration of Glucose Homeostasis in V1a Vasopressin Receptor-Deficient Mice

et al. 2007

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Arginine-vasopressin (AVP) is known to be involved in maintaining glucose homeostasis, and AVP-resistance is observed in poorly controlled non-insulin-dependent diabetes mellitus subjects, resulting in a lowered plasma volume. Recently we reported that V1a vasopressin receptor-deficient (V1aR ؊/؊ ) mice exhibited a decreased circulating blood volume and hypermetabolism of fat accompanied with impaired insulin-signaling. Here we further investigated the roles of the AVP/V1a receptor in regulating glucose homeostasis and plasma volume using V1aR؊/؊ mice. The plasma glucose levels at the baseline or during a glucose tolerance test were higher in V1aR ؊/؊ than wild-type (WT) mice. Moreover, a hyperinsulinemic-euglycemic clamp revealed that the glucose infusion rate was significantly lower in V1aR ؊/؊ mice than in WT mice and that hepatic glucose production was higher in V1aR ؊/؊ mice than WT mice. In contrast to the increased hepatic glucose production, the liver glycogen content was decreased in the mutant mice. These results indicated that the mutant mice had impaired glucose tolerance. Furthermore, feeding V1aR ؊/؊ mice a high-fat diet accompanied by increased calorie intake resulted in significantly overt obesity in comparison with WT mice. In addition, we found that the circulating plasma volume and aldosterone level were decreased in V1aR ؊/؊ mice, although the plasma AVP level was increased. These results suggested that the effect of AVP on water recruitment was disturbed in V1aR ؊/؊ mice. Thus, we demonstrated that one of the AVP-resistance conditions resulting from deficiency of the V1a receptor leads to decreased plasma volume as well as impaired glucose homeostasis, which can progress to obesity under conditions of increased calorie intake. (Endocrinology 148: 2075-2084, 2007)A RGININE-VASOPRESSIN (AVP) is a neuropeptide hormone that is involved in diverse functions, including the regulation of osmotic homeostasis, vasoconstriction, and ACTH release. These physiological effects are mediated by three types of AVP receptors, designated as V1a, V1b, and V2 (1-3). The V1a receptor is widely expressed, whereas the V1b and V2 receptors are predominantly expressed in the anterior pituitary and the kidney, respectively (1-4). The functional role of the V1a receptor is considered to mediate vascular contraction (5), cellular proliferation (6), platelet aggregation (7), and glycogenolysis (1, 8). The V1b receptor stimulates ACTH and insulin release (9, 10). Both V1a and V1b receptors bind to the Gq protein and act through phosphatidylinositol hydrolysis to mobilize intercellular Ca 2ϩ (11,12). The V2 receptor is coupled with the Gs protein and stimulates adenylate cyclase to increase cellular cAMP, which results in the induction of an antidiuretic effect in the kidney (13).There have been several reports indicating the involvement of AVP in regulating the plasma glucose homeostasis. The plasma AVP level was increased in patients with insulindependent diabetes mellitus (IDDM) or non-IDDM (NIDDM) (14, 15), and treati...

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Plasma Arginine Vasopressin in diabetic ketoacidosis

Cited by 46 publications

References 13 publications

Vasopressin and Diabetes mellitus

Vasopressin and Diabetes mellitus

PGE2 receptor EP3 inhibits water reabsorption and contributes to polyuria and kidney injury in a streptozotocin-induced mouse model of diabetes

Alteration of Glucose Homeostasis in V1a Vasopressin Receptor-Deficient Mice

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