Water immersion is associated with an increase in aquaporin-2 excretion in healthy volunteers

Valenti, Giovanna; Fraszl, Waltraud; Addabbo, Francesco; Tamma, Grazia; Procino, Giuseppe; Satta, Ersilia; Cirillo, Massimo; Santo, Natale G. De; Drummer, C.; Bellini, Luigi; Kowoll, R.; Schlemmer, M.; Vogler, Stefan; Kirsch, K.; Svelto, María; Gunga, Hanns‐Christian

doi:10.1016/j.bbamem.2006.03.029

Cited by 12 publications

(12 citation statements)

References 13 publications

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“…Hematocrit increases and there is a decline in mean power and peak power during exercise as well as a greater level of perceived exertion (200). HOWI in warm water has been shown to increase total urinary Aquaporin 2 excretion suggesting elevation of plasma vasopressin levels (391). Forty-five minutes of TN HOWI followed by warm water immersion at 41 • C caused an immediate decrease of plasma fibrinogen and plasminogen activator inhibitor activity concentration decreased immediately.…”

Section: Head-out Water Immersion In Warm Watermentioning

confidence: 97%

Human Physiology in an Aquatic Environment

Pendergast

Moon

Krasney

et al. 2015

Comprehensive Physiology

134

137

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Water covers over 70% of the earth, has varying depths and temperatures and contains much of the earth's resources. Head-out water immersion (HOWI) or submersion at various depths (diving) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and renal responses. The translocation of blood into the thorax and elevation of plasma volume by autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which result in endocrine changes that return plasma volume and arterial pressure to preimmersion levels. Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output compared to TN; however, they influence heart rate and the distribution of muscle and fat blood flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The properties of water determine the mechanical load and the physiological responses during exercise in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac output. During submersion, compressed gas must be breathed which introduces the potential for oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompression and after may cause pain in joints and the nervous system.

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Section: Head-out Water Immersion In Warm Watermentioning

confidence: 97%

Human Physiology in an Aquatic Environment

Pendergast

Moon

Krasney

et al. 2015

Comprehensive Physiology

134

137

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“…To this end, urine samples were spun down at 3,000 rpm for 10 min at 4°C to remove cellular debris in the presence of the following protease inhibitors: 2 m M phenylmethylsulphonyl fluoride, 1 µg/ml leupeptin, 1 µg/ml pepstatin. AQP2 excretion was measured, as previously described, by ELISA [22]. Five or 10 µl of urine sample were diluted to 50 µl in PBS containing 0.01% SDS, placed in a MaxiSorp 96-well microplate (Nunc, Rochester, N.Y., USA) and incubated for 16 h at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Two Novel Missense Mutations in the <i>AQP2 </i>Gene Causing Nephrogenic Diabetes Insipidus

et al. 2006

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Here, we report the aquaporin 2 (AQP2) mutational analysis of a patient with nephrogenic diabetes insipidus heterozygote due to two novel missense mutations. Direct sequencing of DNA in the male patient revealed that he was compound heterozygote for two mutations in the AQP2 gene: a thymine-to-adenine transversion at position 450 (c.450T>A) in exon 2 and a guanine-to-thymine at nucleotide position 643 (c.643G>T) in exon 4. The double heterozygous 450T>A and 643G>T transversion causes the amino acid substitution D150E and G215C. Direct sequencing of exons 2 and 4 of the AQP2 gene from each of the parents revealed that the c.450T>A mutation was inherited from the father while the c.643G>T mutation was inherited from the mother. Analysis of AQP2 excretion demonstrated that no AQP2 was detectable in the urine of the proband, whereas normal AQP2 levels were measured in both parents. When expressed in renal cells, both proteins were retarded in the endoplasmic reticulum and no redistribution was observed after forskolin stimulation. Of note, homology modeling revealed that the two mutations involve two highly conserved residues providing important clues about the role of the wt residues in AQP2 stability and function.

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“…AQP2 is a well-established urinary biomarker of CD responsiveness to AVP and is critical for the diagnosis of several disorders of renal water balance [31][32][33][34][35]. U-AQP2 reflects its abundance on the apical membrane [33][34][35]. Accordingly, u-AQP2 increases during thirsting and after DDAVP administration, and decreases after a WL [30].…”

Section: Citationmentioning

confidence: 99%

“…AVP, upon binding to the V2 receptor (V2R), increases CD water permeability by promoting the trafficking of AQP2 from intracellular storage vesicles to the apical membrane, in the short term. AQP2 is a well-established urinary biomarker of CD responsiveness to AVP and is critical for the diagnosis of several disorders of renal water balance [31][32][33][34][35]. U-AQP2 reflects its abundance on the apical membrane [33][34][35].…”

Section: Citationmentioning

confidence: 99%

Knockdown of the BBS10 Gene Product Affects Apical Targeting of AQP2 in Renal Cells: A Possible Explanation for the Polyuria Associated with Bardet-Biedl Syndrome

Zacchia¹

2014

J Genet Syndr Gene Ther

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Water immersion is associated with an increase in aquaporin-2 excretion in healthy volunteers

Abstract: Here, we report the alterations in renal water handling in healthy volunteers during a 6 h thermoneutral water immersion at 34 to 36 degrees C. We found that water immersion is associated with a reversible increase in total urinary AQP2 excretion.

Cited by 12 publications

References 13 publications

Human Physiology in an Aquatic Environment

Human Physiology in an Aquatic Environment

Characterization of Two Novel Missense Mutations in the <i>AQP2 </i>Gene Causing Nephrogenic Diabetes Insipidus

Knockdown of the BBS10 Gene Product Affects Apical Targeting of AQP2 in Renal Cells: A Possible Explanation for the Polyuria Associated with Bardet-Biedl Syndrome

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