Vasopressin and Diabetes mellitus

Bankir, Lise; Bardoux, Pascale; Ahloulay, Mina

doi:10.1159/000045879

Cited by 100 publications

(68 citation statements)

References 57 publications

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“…Thus, it is logical to hypothesize that the association between the effects of hyperglycemia may, at least in part, affect the occurrence of nocturia. In addition, the lack of arginine vasopressin (AVP) secretion and renal AVP resistance induced by diabetes may play a crucial role (20,21). People with obesity (BMI of > 27 kg/m 2 ) had higher odds for suffering from nocturia, as compared to those without obesity, which was consistent with numerous epidemiological studies (5,7,8,15,17).…”

Section: Discussionsupporting

confidence: 74%

Prevalence and risk factors for nocturia in middle-aged and elderly people from public health centers in Taiwan

et al. 2012

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Purpose: To assess the occurrence and the associated risk factors for nocturia among middle-aged and elderly people from public health centers in southern Taiwan. Materials and Methods: Data were part of our previous cross-sectional study which used a self-administered questionnaire for the assessment of lower urinary tract symptoms. A total of 1011 responders who were at least 40 years of age were enrolled from any of four local public health centers for any reason in Pingtung County, Taiwan. Nocturia, as a dependent variable, was defi ned as two or more episodes per night. Covariables included age, gender, and chronic illnesses (obesity, hypertension, diabetes, cardiovascular disease, and stroke). Multivariate logistic regression was applied to determine the risk factors associated with nocturia. A p-value of less than 0.05 was considered statistically signifi cant. Results: About 38.1% (385/1011) of the participants reported having nocturia  2 episodes/night, and the occurrence of nocturia increased with advanced age. More than half (51.2%, 197/385) participants with nocturia perceived at least "a bit of a problem" on the sleep quality. The multivariate logistical regression showed that the independent risk factors for nocturia were age (OR:1.06, CI:1.05-1.08), hypertension (OR:1.58, CI:1.16-2.16) and diabetes (OR:1.59, CI:1.03-2.45) and obesity (OR:1.47, CI:1.02-2.10), while a borderline effect on nocturia was produced by cardiovascular disease (OR:1.66, CI: 0.98-2.79) and stroke (OR:2.75, CI:0.88-8.64). Conclusions: Several chronic illnesses coexisted with nocturia. Health care providers need to be aware of an increased risk of nocturia among people with certain chronic illnesses, and provide appropriate health care.

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Section: Discussionsupporting

confidence: 74%

Prevalence and risk factors for nocturia in middle-aged and elderly people from public health centers in Taiwan

et al. 2012

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“…Moreover, an imbalance in the relative abundance, sensitivity, affinity, and/or signal transduction of V2 versus V1a receptors in some disease states might alter the normal balance between V2 and V1a influences. Noteworthy, studies in rats have shown that V1a but not V2 receptors are downregulated (44,45) in situations in which vasopressin levels are increased, such as in diabetes (46). This study explored only the acute effects of V2 agonism and does not allow extrapolation to chronic situations, but a few experimental studies suggest that chronic V2 receptor-induced excessive sodium reabsorption could lead to sodium retention and to a compensatory rise in BP.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Bankir

Fernandes

Bardoux

et al. 2005

Journal of the American Society of Nephrology

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121

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In addition to its effect on water permeability, vasopressin, through its V2 receptors (AVPR2), stimulates Na reabsorption in the collecting duct by increasing the activity of the amiloride-sensitive sodium channel ENaC. This study evaluated whether dDAVP (a potent AVPR2 agonist) reduces sodium excretion in healthy humans (n ‫؍‬ 6) and in patients with central (C; n ‫؍‬ 2) or nephrogenic (N) diabetes insipidus (DI) as a result of mutations of either the aquaporin 2 gene (AQP2; n ‫؍‬ 3) or AVPR2 (n ‫؍‬ 10). dDAVP was infused intravenously (0.3 g/kg body wt in 20 min), and urine was collected for 60 min before (basal) and 150 min after the infusion. dDAVP markedly reduced both urine flow rate and sodium excretion in healthy individuals. A reduction in sodium excretion was also observed in CDI and NDI-AQP2 patients but not in NDI-AVPR2 patients. The magnitude of the fall in sodium excretion correlated with the rise in urine osmolality and the fall in urine output but not with the simultaneously observed fall in mean BP. These results suggest that the dDAVP-induced antinatriuresis is due to a direct V2 receptor-dependent stimulation of sodium reabsorption in the collecting duct and is not secondary to a hemodynamic effect. In conclusion, this study reveals a potent V2-dependent antinatriuretic effect of vasopressin in humans. The possibility that an inappropriate stimulation of ENaC by vasopressin might lead to significant sodium retention in chronic situations remains to be determined. 16: 192016: -192816: , 200516: . doi: 10.1681 I nappropriate retention of sodium and water by the kidney is thought to be a key factor in several forms of hypertension. Thus, it is important to identify factors that may favor excessive sodium reabsorption by the kidney. Vasopressin is known to promote water conservation by increasing the permeability to water of the collecting ducts (CD), thus allowing osmotically driven water reabsorption along these ducts when dilute distal tubular fluid enters them in the cortex and later when they traverse the hyperosmotic medulla. However, the effect of vasopressin on sodium excretion is less clear. A large number of studies have shown that vasopressin infusion increases sodium excretion in vivo in rats, dogs, and sheep (e.g., references 1-4). This natriuretic effect is difficult to reconcile with the fact that, in vitro, vasopressin stimulates sodium reabsorption in the isolated perfused CD (5,6), in the amphibian bladder (a tissue that shares a number of similarities with the mammalian CD) (7), and in several cell lines issued from these two tissues (8 -10). This effect on sodium reabsorption is inhibitable by amiloride and has been shown to result from activation of the endothelial sodium channel ENaC (11). Moreover, chronic elevation of vasopressin or infusion of its V2 agonist dDAVP (12) has been shown to increase the abundance of mRNA (13) and protein (14) of the ␤ and ␥ subunits of ENaC and to enhance markedly the subsequent functional response (water and sodium reabsorption) to exoge...

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“…Type I diabetes has been associated with natriuresis and diuresis, as well as activation of vasopressin and the reninangiotensin-aldosterone system (7,84). Several groups have examined the regulation of sodium transporters in type I diabetic rodents (47,57,91,92,97,109,124).…”

Section: Altered Expression Of Sodium Transporter and Channels In Diamentioning

confidence: 99%

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

Tiwari

Riazi²,

Ecelbarger³

2007

American Journal of Physiology-Renal Physiology

111

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Insulin has been shown to have antinatriuretic actions in humans and animal models. Moreover, endogenous hyperinsulinemia and insulin infusion have been correlated to increased blood pressure in some models. In this review, we present the current state of understanding with regard to the regulation of the major renal sodium transporters by insulin in the kidney. Several groups, using primarily cell culture, have demonstrated that insulin can directly increase activity of the epithelial sodium channel, the sodium-phosphate cotransporter, the sodium-hydrogen exchanger type III, and Na-K-ATPase. We and others have demonstrated alterations in the expression at the protein level of many of these same proteins with insulin infusion or in hyperinsulinemic models. We also discuss how this regulation is perturbed in type I and type II diabetes mellitus. Finally, we discuss a potential role for regulation of insulin receptor signaling in the kidney in contributing to sodium balance and blood pressure. insulin resistance; ENaC; Zucker rats; streptozotocin Overview INSULIN HAS BEEN DEMONSTRATED to increase sodium reabsorption in the proximal tubule (9), the thick ascending limb (78, 102), and the distal tubule including the collecting duct (54, 144), using micropuncture and perfused tubule approaches. Over 10 years ago, Sechi (127), Butlen (30), and colleagues using I 125 -labeled insulin demonstrated binding sites in multiple cell types along the renal tubular epithelium. However, because the kidney expresses other receptors similar to the classic insulin receptor (IR), including the insulin growth factor receptor (IGF) and the IR-related receptor (IRR), the precise nature of the "receptor" that labeled insulin was binding to was not absolutely certain. Nonetheless, more recent studies showed mRNA expression of the classic IR in whole homogenates of the kidney (31, 32,130,132), and our group (150) has recently found IR expression at the protein level using immunoblotting and immunohistochemistry in the proximal tubule, thick ascending limb, and collecting duct. In this review, we discuss studies that have investigated the regulation of the major renal sodium transporters in the kidney by insulin. In addition, we examine how this regulation is altered in insulin resistance, which is a hyperinsulinemic state, as well as in type I and type II diabetes. We also discuss what is known about the regulation of the IR in the kidney, how it is affected by insulin resistance and/or diabetes, and how this might ultimately affect sodium balance and blood pressure.

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Vasopressin and Diabetes mellitus

Cited by 100 publications

References 57 publications

Prevalence and risk factors for nocturia in middle-aged and elderly people from public health centers in Taiwan

Prevalence and risk factors for nocturia in middle-aged and elderly people from public health centers in Taiwan

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

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