Upregulation of aquaporin 2 water channel expression in pregnant rats.

Ohara, Miho; Martin, Pierre‐Yves; Xu, Dingli; John, Joseph; Pattison, Tim; Kim, J K; Schrier, Robert W.

doi:10.1172/jci649

Cited by 101 publications

(70 citation statements)

References 31 publications

(32 reference statements)

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“…The dose of OPC-31260 used in our study was able to inhibit VP activity, because both urine volume and urine osmolality were significantly changed in both groups of animals (Table 1), consistent with previous data by Ohara et al (18).…”

Section: Discussionsupporting

confidence: 92%

“…OPC-31260 was given by subcutaneous injection (15 mg/kg twice a day for 3 days for a total of 6 injections). This dose has been proven to inhibit VP effects in normal rats (18). Body weight and water ingestion in each rat were measured twice daily during 4 days before the study and were expressed as the mean of all observations.…”

Section: Methodsmentioning

confidence: 99%

“…OPC-31260 is a nonpeptide V 2 -receptor inhibitor developed by Yamamura et al (21), and its actions are limited to states where VP activity is present. This approach was recently used by Ohara et al (18), who were able to show a VP-mediated upregulation of the aquaporin-2 water channel in pregnant rats by using OPC-31260.…”

mentioning

confidence: 99%

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Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla

Bertuccio

Ibarra

Toledo

et al. 2002

American Journal of Physiology-Renal Physiology

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Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V 2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 Ϯ 1.5 to 3.7 Ϯ 0.8 in controls (P Ͻ 0.05) and from 19.0 Ϯ 0.8 to 2.9 Ϯ 0.5 mol P i ⅐ mg protein Ϫ1 ⅐ h Ϫ1 in moderate CRF rats (P Ͻ 0.05). CRF was associated with a significant increase in Na-K-ATPase activity (P Ͻ 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 Ϯ 21.5% compared with controls (P Ͻ 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 Ϯ 9.5 and 105.3 Ϯ 10.9%, respectively (P Ͻ 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 Ϯ 6.5 and 30.0 Ϯ 6.9%, respectively (P Ͻ 0.05), and was not influenced by CRF (95.7 Ϯ 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.vasopressin; rbsc-1; sodium-potassium-adenosine 5Ј-triphosphatase; chronic renal failure THERE IS STRONG EVIDENCE that vasopressin (VP) stimulates Na-K-ATPase and Na ϩ -K ϩ -Cl Ϫ cotransporter in the kidney outer medulla and, more precisely, in the medullary thick ascending limb of Henle (mTAL) (15). However, the experimental designs so far have been mostly related to the administration of exogenous VP, to either intact animals or in vitro preparations. The question of whether the level of endogenous VP activity plays a homeostatic role at the kidney outer medulla has not yet been examined. The introduction of powerful VP inhibitors has made it possible to design experiments looking at that question. OPC-31260 is a nonpeptide V 2 -receptor inhibitor developed by Yamamura et al. (21), and its actions are limited to states where VP activity is present. This approach was recently used by Ohara et al. (18), who were able to show a VP-mediated upregulation of the aquaporin-2 water channel in pregnant rats by using OPC-31260.In addition, previous experiments from our laboratory and those of others have suggested that in chronic renal failure the remaining nephrons suffer diverse adaptive mechanisms. Thus Bertuccio et al. (1, 2) showed an increase in intracellular cAMP levels in microdissected mTAL segments in chronic renal failure (CRF) rats, which were unresponsive to VP in vitro, opposed to baseline lower levels and a dose-respon...

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

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Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla

Bertuccio

Ibarra

Toledo

et al. 2002

American Journal of Physiology-Renal Physiology

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“…AQP2, an AVP-sensitive collecting duct water channel, has been shown to increase in the kidney medullary papillae during pregnancy. This observation was made in the presence of normal levels of circulating AVP, suggesting a non-AVP dependent mechanism of action during gestation (24) or resetting of the AVP-AQP2 regulation in pregnancy. One would expect that, in the presence of increased AVP, water permeability would increase by upregulating the AQP2 channel.…”

Section: Discussionmentioning

confidence: 72%

Angiotensin-(1-7) serves as an aquaretic by increasing water intake and diuresis in association with downregulation of aquaporin-1 during pregnancy in rats

Joyner¹,

Neves²,

Stovall³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Joyner J, Neves LAA, Stovall K, Ferrario CM, Brosnihan KB. Angiotensin-(1-7) serves as an aquaretic by increasing water intake and diuresis in association with downregulation of aquaporin-1 during pregnancy in rats. Am J Physiol Regul Integr Comp Physiol 294: R1073-R1080, 2008. First published January 9, 2007 doi:10.1152/ajpregu.00572.2007.-We previously demonstrated that kidney and urine levels of angiotensin-(1-7) [ANG-(1-7)] were increased in pregnancy. To explore the role of ANG-(1-7) on fluid and electrolyte homeostasis during pregnancy, we evaluated the effect of the ANG-(1-7) antagonist D-alanine-[ANG-(1-7)] (A-779) on kidney function. Virgin and pregnant rats received infusion of vehicle or A-779 (48 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) for 8 days by osmotic minipumps. Metabolic studies were done on treatment day 7-8. Virgin and pregnant rats at day 15 and 19 were killed, and blood and kidneys were collected. Kidneys were prepared for Western blot analysis for aquaporin-1 (AQP1) and aquaporin-2. In virgin female rats, A-779 increased urine volume and decreased urinary osmolality and AQP1 with no change in water intake. In 19-day pregnant rats, A-779 significantly decreased water intake and urine volume and increased urinary osmolality and kidney AQP1 expression. Only in late gestation did A-779 treatment decrease the difference between intake and output (balance). A-779 treatment increased plasma vasopressin in late gestation but did not change vasopressin in virgins. In virgin and pregnant animals, A-779 administration had no effect on blood pressure, plasma volume, blood volume, or urinary electrolytes. These results suggest that ANG-(1-7) produces antidiuresis associated with upregulation of AQP1 in virgin rats, whereas ANG-(1-7) produces diuresis in late gestation with downregulation of AQP1. ANG-(1-7) contributes to the enhanced water intake during pregnancy, allowing maintenance of the normal volume-expanded state despite diuresis produced in part by decreased AVP and AQP1. renin-angiotensin system; pregnancy; angiotensin-(1-7); D-alanine-[angiotensin-(1-7)]; D-alanine; aquaporin; vasopressin NORMAL PREGNANCY IS A physiological condition characterized by hemodynamic change, including increased cardiac output and hypervolemia, decreased total peripheral resistance, and decreased or normal blood pressure (2). The renin angiotensin system (RAS), which is involved in blood pressure regulation and salt and fluid homeostasis, is markedly increased during pregnancy, as evidenced by increased circulating concentration of angiotensinogen, renin activity, and angiotensin II (ANG II; see Refs. 2,5,and 20). Also, increased during normal pregnancy is angiotensin-(1-7) [ANG-(1-7)], the active vasodilator of the RAS. Urinary excretion of ANG-(1-7) rises progressively during human pregnancy to levels that are 20-fold higher by the end of gestation compared with the normal menstrual cycle (35). Urinary ANG-(1-7) concentration is also increased with gestation in rats (22). ANG-(1-7), along with its forming enzyme angiotensin conver...

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“…Congestive heart failure is a life-threatening complication of coronary vascular disease caused by excessive retention of water. Increased expression of AQP2 has been found in rat models of congestive heart failure and is also believed to explain fluid retention in pregnancy (24,25).…”

Section: Mammalian Homologsmentioning

confidence: 99%

The Aquaporins, Blueprints for Cellular Plumbing Systems

Agre

Bonhivers²,

Borgnia³

1998

Journal of Biological Chemistry

425

281

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Membrane Water PermeabilityPlasma membranes provide an effective barrier to the extracellular environment. Water was long believed to move through lipid bilayers by simple diffusion; however, membranes from different tissues vary in their permeability to water. The variability is particularly evident in mammalian kidney where proximal tubules and descending thin limbs of Henle's loop have constitutively high water permeability and are responsible for reabsorption of more than 150 liters per day in adult humans. In contrast, ascending thin limbs have very low water permeability. Renal distal tubules empty into collecting ducts where stimulation with vasopressin causes an increase in water permeability (see Ref. 1 for review). These observations led to the suggestion that specialized water transport molecules must exist in membranes with intrinsically high water permeability. Nevertheless, despite extensive studies, the molecular identity of water transport proteins remained elusive until recently.The well defined features of membrane water permeability permitted serendipitous identification of the first known water channel. While purifying the 32-kDa subunit of the red cell Rh blood group antigen, a new 28-kDa polypeptide was discovered (2). Detailed biochemical studies of this newly identified tetrameric membrane protein were made easy by its low solubility in N-lauroylsarcosine, which permitted simple purification (3). The abundance of the protein in rat renal proximal tubules and descending thin limbs (2) sparked the idea that the 28-kDa polypeptide may be the long sought water channel, and its unique N-terminal amino acid sequence permitted cloning from an erythroid cDNA library (4). Functional Analyses of AQP1The Xenopus oocyte expression system has been extremely useful for study of water transport. Oocytes injected with cRNA for the 28-kDa polypeptide exhibit remarkably high osmotic water permeability (P f ϳ200 ϫ 10 Ϫ4 cm s Ϫ1) and rapidly explode in hypotonic buffer (Fig. 1), whereas control oocytes exhibit minimal permeability (5). First referred to as "CHIP28," this protein is now designated aquaporin-1 (AQP1) 1 by the Human Genome Nomenclature Committee (see http://www.gene.ucl.ac.uk/nomenclature). Despite its large water permeability, AQP1 failed to confer a measurable increase in membrane currents (5). Consistent with these results, highly purified AQP1 protein reconstituted into proteoliposomes exhibits high unit water permeability (P f ϳ3 ϫ 10 9 water molecules subunit Ϫ1 s Ϫ1 ), whereas permeation by other small solutes or even protons was undetectable (6). The prevailing view is that AQP1 is a constitutively active, water-selective pore that permits osmotically driven movement of water. A report that forskolin induces a cation current in AQP1-expressing oocytes (7) was not reproduced by multiple other scientific groups. Permeation by CO 2 has recently been proposed, because rates of pH change are about 40% higher in oocytes expressing AQP1 (8). Permeation by O 2 , nitric oxide, and other gases is...

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Upregulation of aquaporin 2 water channel expression in pregnant rats.

Cited by 101 publications

References 31 publications

Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla

Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla

Angiotensin-(1-7) serves as an aquaretic by increasing water intake and diuresis in association with downregulation of aquaporin-1 during pregnancy in rats

The Aquaporins, Blueprints for Cellular Plumbing Systems

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Upregulation of aquaporin 2 water channel expression in pregnant rats.

Cited by 101 publications

References 31 publications

Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl−cotransporterrbsc-1in rat outer medulla

Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl−cotransporterrbsc-1in rat outer medulla

Angiotensin-(1-7) serves as an aquaretic by increasing water intake and diuresis in association with downregulation of aquaporin-1 during pregnancy in rats

The Aquaporins, Blueprints for Cellular Plumbing Systems

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Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla

Endogenous vasopressin regulates Na-K-ATPase and Na⁺-K⁺-Cl⁻cotransporterrbsc-1in rat outer medulla