Physiology and pathophysiology of renal aquaporins

Kwon, Tae‐Hwan; Hager, Henrik; Nejsum, Lene N.; Andersen, M L; Frøkiær, Jørgen; Nielsen, Søren

doi:10.1053/snep.2001.21647

Cited by 68 publications

(39 citation statements)

References 79 publications

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“…1A) in the kidney in response to NS venom. AQP4 is expressed in the basolateral plasma membranes of collecting duct principal cells and is the main exit pathway for water reabsorbed by AQP2 [45], and its decreased expression may result in polyuria during envenomation. The kidney showed the second greatest changes in gene expression amongst the organs (50 genes differentially regulated).…”

Section: Discussionmentioning

confidence: 99%

Molecular basis of cardiotoxicity upon cobra envenomation

Cher

Armugam

Zhu

et al. 2005

CMLS, Cell. Mol. Life Sci.

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Various clinical manifestations leading to death have been documented in most cases of bites caused by venomous snakes. Cobra envenomation is an extremely variable process and known to cause profound neurological abnormalities. The complexity of cobra venom can induce multiple-organ failure, leading to death in case of severe envenomation. Intramuscular administration of Malayan spitting cobra (Naja sputatrix) crude venom at 1 microg/g dose caused death in mice in approximately 3 h. Analysis of gene expression profiles in the heart, brain, kidney, liver and lung revealed 203 genes whose expression was altered by at least 3-fold in response to venom treatment. Of these, 50% were differentially expressed in the heart and included genes involved in inflammation, apoptosis, ion transport and energy metabolism. Electrocardiogram recordings and serum troponin T measurements indicated declining cardiac function and myocardial damage. This not only sheds light on the cardiotoxicity of cobra venom but also reveals the molecular networks affected during envenomation.

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Section: Discussionmentioning

confidence: 99%

Molecular basis of cardiotoxicity upon cobra envenomation

Cher

Armugam

Zhu

et al. 2005

CMLS, Cell. Mol. Life Sci.

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“…Among these, AQP2, localized in the luminal membrane of the principal cells of the collecting duct, is the chief target for the shortterm regulation of the collecting duct permeability by vasopressin. AQP2, and also AQP3 and AQP4 (basolateral water channels of the collecting duct), are regulated via the long-term effects of chronic dehydration that change the total abundance of these three channels in collecting duct cells ( Figure 1a) (Yamamoto et al, 1995;Ishibashi et al, 1997;Murillo-Carretero et al, 1999;Kwon et al, 2001) (the effect on AQP3 is only partially mediated by stimulating vasopressin V2 receptors). As urinary AQP2 excretion is very low compared to the total AQP2 in the kidney (E3%), it may not reflect intrarenal changes in the protein.…”

Section: Renal Consequences Of a High Level Of Vasopressin In A Healtmentioning

confidence: 99%

Mild dehydration, vasopressin and the kidney: animal and human studies

Bouby

Fernandes

2003

Eur J Clin Nutr

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Water balance depends essentially on fluid intake and urine excretion. Mild dehydration and the consequent hypertonicity of the extracellular fluid induce an increase in vasopressin secretion, thus stimulating urine concentrating processes and the feeling of thirst. The osmotic threshold for the release of vasopressin is lower than that for thirst and also shows appreciable individual variation. Sustained high levels of vasopressin and low hydration induce morphological and functional changes in the kidney. However, they could also be risk factors in several renal disorders, such as chronic renal failure, diabetic nephropathy and saltsensitive hypertension.

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“…In the kidney, AQP-1, -2, -3, -4, -6, -7 and -8 are expressed with different segmental localization (Elkjaer et al, 2001;Kwon et al, 2001). AQP-1 is expressed in the apical and basolateral membranes, whereas AQP-3 and -4 are only present in the basolateral membrane (Deen and van Os, 1998).…”

mentioning

confidence: 99%

Claudin-2, a component of the tight junction, forms a paracellular water channel

Rosenthal

Milatz

Krug

et al. 2010

Journal of Cell Science

371

330

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SummaryWhether or not significant amounts of water pass the tight junction (TJ) of leaky epithelia is still unresolved, because it is difficult to separate transcellular water flux from TJ-controlled paracellular water flux. Using an approach without differentiating technically between the transcellular and paracellular route, we measured transepithelial water flux with and without selective molecular perturbation of the TJ to unequivocally attribute changes to the paracellular pathway. To this end, MDCK C7 cells were stably transfected with either claudin-2 or claudin-10b, two paracellular cation-channel-forming TJ proteins that are not endogenously expressed in this cell line. Claudin-2 is typical of leaky, water-transporting epithelia, such as the kidney proximal tubule, whereas claudin-10b is present in numerous epithelia, including water-impermeable segments of the loop of Henle. Neither transfection altered the expression of endogenous claudins or aquaporins. Water flux was induced by an osmotic gradient, a Na + gradient or both. Under all conditions, water flux in claudin-2-transfected cells was elevated compared with vector controls, indicating claudin-2-mediated paracellular water permeability. Na + -driven water transport in the absence of an osmotic gradient indicates a single-file mechanism. By contrast, claudin-10b transfection did not alter water flux. We conclude that claudin-2, but not claudin-10b, forms a paracellular water channel and thus mediates paracellular water transport in leaky epithelia.

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Physiology and pathophysiology of renal aquaporins

Cited by 68 publications

References 79 publications

Molecular basis of cardiotoxicity upon cobra envenomation

Molecular basis of cardiotoxicity upon cobra envenomation

Mild dehydration, vasopressin and the kidney: animal and human studies

Claudin-2, a component of the tight junction, forms a paracellular water channel

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