Vasopressin–aquaporin-2 pathway: recent advances in understanding water balance disorders

Ranieri, Marianna; Mise, Annarita Di; Tamma, Grazia; Valenti, Giovanna

doi:10.12688/f1000research.16654.1

Cited by 41 publications

(42 citation statements)

References 125 publications

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“…Aquaporin-2 (AQP2) is a vasopressin-regulated water channel that mediates water absorption in renal collecting ducts, therefore allowing urine concentration and the adequate maintenance of body water homeostasis (Ranieri, Di Mise, Tamma, & Valenti, 2019). Under physiological conditions, circulating vasopressin binds to type 2 vasopressin receptor, which is located on the basolateral membrane of principal cells and triggers a well-established signaling pathway (Knepper & Inoue, 1997).…”

Section: Introductionmentioning

confidence: 99%

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration

Giusto

Pizzoni

Rivarola

et al. 2019

Journal Cellular Physiology

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Aquaporin-2 (AQP2) promotes renal cell migration by the modulation of integrin β1 trafficking and the turnover of focal adhesions. The aim of this study was to investigate whether AQP2 also works in cooperation with Na + /H + exchanger isoform 1 (NHE1), another well-known protein involved in the regulation of cell migration.Our results showed that the lamellipodia of AQP2-expressing cells exhibit significantly smaller volumes and areas of focal adhesions and more alkaline intracellular pH due to increased NHE1 activity than AQP2-null cells. The blockage of AQP2, or its physically-associated calcium channel TRPV4, significantly reduced lamellipodia NHE1 activity. NHE1 blockage significantly reduced the rate of cell migration, the number of lamellipodia, and the assembly of F-actin only in AQP2expressing cells. Our data suggest that AQP2 modulates the activity of NHE1 through its calcium channel partner TRPV4, thereby determining pH-dependent actin polymerization, providing mechanical stability to delineate lamellipodia structure and defining the efficiency of cell migration.

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Section: Introductionmentioning

confidence: 99%

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration

Giusto

Pizzoni

Rivarola

et al. 2019

Journal Cellular Physiology

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“…AQP2 is translocated to the apical membrane in the renal collecting duct, triggered upon detection by vasopressin receptor 2. AVP is secreted from the pituitary gland with an increase in plasma osmotic pressure, and water is reabsorbed via AQP2 to regulate the body fluid volume [34,35]. Urine AQP2 is known to correlate with the amount of AQP2 translocated to the membrane and is used as an indicator of the reabsorption of water [36,37].…”

Section: Discussionmentioning

confidence: 99%

Effect of Increased Daily Water Intake and Hydration on Health in Japanese Adults

et al. 2020

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Increased hydration is recommended as healthy habit with several merits. However, supportive data are sparse. To assess the efficacy of increased daily water intake, we tested the effect of water supplementation on biomarkers in blood, urine, and saliva. Twenty-four healthy Japanese men and 31 healthy Japanese women with fasting blood glucose levels ranging from 90–125 mg/dL were included. An open-label, two-arm, randomized controlled trial was conducted for 12 weeks. Two additional 550 mL bottles of water on top of habitual fluid intake were consumed in the intervention group. The subjects drank one bottle of water (550 mL) within 2 h of waking, and one bottle (550 mL) 2 h before bedtime. Subjects increased mean fluid intake from 1.3 L/day to 2.0 L/day, without changes in total energy intake. Total body water rate increased with associated water supplementation. There were no significant changes in fasting blood glucose and arginine vasopressin levels, but systolic blood pressure was significantly decreased in the intervention group. Furthermore, water supplementation increased body temperature, reduced blood urea nitrogen concentration, and suppressed estimated glomerular filtration rate reduction. Additionally, existence of an intestinal microbiome correlated with decreased systolic blood pressure and increased body temperature. Habitual water supplementation after waking up and before bedtime in healthy subjects with slightly elevated fasting blood glucose levels is not effective in lowering these levels. However, it represents a safe and promising intervention with the potential for lowering blood pressure, increasing body temperature, diluting blood waste materials, and protecting kidney function. Thus, increasing daily water intake could provide several health benefits.

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“…If the water content in the body is low, AVP binds to its type 2 receptor (V2R) localized in the basal cell membrane of collecting duct principal cells and stimulates the expression of aquaporin-2 (AQP2) water channels. Furthermore, AVP triggers a signaling cascade leading to the accumulation of AQP2 in the apical membrane (for a detailed review see [11,41]). This mechanism enables reabsorption of electrolyte-free water from the intraluminal urine and forms the basis of urinary concentrating ability.…”

Section: The Collecting Duct Epithelial Barrier In Electrolyte-free Wmentioning

confidence: 99%

Claudins in the Renal Collecting Duct

Leiz

Schmidt‐Ott

2019

IJMS

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The renal collecting duct fine-tunes urinary composition, and thereby, coordinates key physiological processes, such as volume/blood pressure regulation, electrolyte-free water reabsorption, and acid-base homeostasis. The collecting duct epithelium is comprised of a tight epithelial barrier resulting in a strict separation of intraluminal urine and the interstitium. Tight junctions are key players in enforcing this barrier and in regulating paracellular transport of solutes across the epithelium. The features of tight junctions across different epithelia are strongly determined by their molecular composition. Claudins are particularly important structural components of tight junctions because they confer barrier and transport properties. In the collecting duct, a specific set of claudins (Cldn-3, Cldn-4, Cldn-7, Cldn-8) is expressed, and each of these claudins has been implicated in mediating aspects of the specific properties of its tight junction. The functional disruption of individual claudins or of the overall barrier function results in defects of blood pressure and water homeostasis. In this concise review, we provide an overview of the current knowledge on the role of the collecting duct epithelial barrier and of claudins in collecting duct function and pathophysiology.Structurally, the transmembrane proteins connect in both cis and trans to neighboring claudins of the same, as well as the opposing, cell membranes forming TJ strands [9]. Claudins are sufficient to arrange those strands when expressed in cells lacking endogenous TJ formation [10].Here, we review the role of claudins in epithelial barrier formation with emphasis on the renal collecting duct as well as their implications in collecting duct physiology and function. The Renal Collecting DuctThe renal collecting duct is the most distal part of the renal tubules. It connects renal nephrons with the renal pelvis and-together with the distal convoluted tubule and the connecting tubule-it contributes to the aldosterone-sensitive distal nephron. In general, the renal collecting duct plays important roles in fine-tuning urinary composition, extracellular fluid volume, electrolyte balance, blood pressure regulation, water homeostasis, and acid-base regulation [11,12].Although most of the water and solute reabsorption in the kidney occurs in the more upstream segments of the nephron, transport variability in the renal collecting duct is significantly higher, and ion and water transport are under strict hormonal control [11]. This permits to adjust reabsorption and secretion to prevalent physiological conditions and to control the body's water and electrolyte balance closely.The main solutes reabsorbed in the collecting duct are sodium (Na+) and chloride (Cl−), while potassium (K+) is secreted into the urine [13] (Figure 1). Transport of these ions occurs via the transcellular route-mediated by channels and membrane transporters-and via the paracellular route-mediated by TJs.

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Vasopressin–aquaporin-2 pathway: recent advances in understanding water balance disorders

Cited by 41 publications

References 125 publications

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration

Effect of Increased Daily Water Intake and Hydration on Health in Japanese Adults

Claudins in the Renal Collecting Duct

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Vasopressin–aquaporin-2 pathway: recent advances in understanding water balance disorders

Cited by 41 publications

References 125 publications

Aquaporin‐2 and Na+/H+ exchanger isoform 1 modulate the efficiency of renal cell migration

Aquaporin‐2 and Na+/H+ exchanger isoform 1 modulate the efficiency of renal cell migration

Effect of Increased Daily Water Intake and Hydration on Health in Japanese Adults

Claudins in the Renal Collecting Duct

Contact Info

Product

Resources

About

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration

Aquaporin‐2 and Na⁺/H⁺ exchanger isoform 1 modulate the efficiency of renal cell migration