Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Men tend to dehydrate more than women after prolonged exercise, possibly due to lower water intake and higher perspiration rate. Women are prone to exercise-associated hyponatremia, primarily attributed to the higher water consumption causing hypervolemia. Since aquaporin-2 (AQP2) water channels in the kidney collecting duct (CD) principal cells (PCs) are involved in maintaining water balance, we investigated their role in sex-dependent water homeostasis in wild-type (WT) C57BL/6 mice. Because CD intercalated cells (ICs) may also be involved in water balance, we also assessed the urine concentrating ability of V-ATPase B1 subunit-deficient (Atp6v1b1-/-) mice. Upon 12-hour water deprivation, urine osmolality increased by 59% in WT female mice and by only 28% in males. This difference was abolished in Atp6v1b1-/- mice, in which dehydration induced a ~30% increase in urine osmolarity in both sexes. AQP2 levels were highest in WT females; female Atp6v1b1-/- mice had substantially lower AQP2 expression than WT females, comparable to the low AQP2 levels seen in both Atp6v1b1-/- and WT males. After dehydration, AQP2 relocates towards the PC apical pole, especially in the inner stripe and inner medulla, and to a greater extent in WT females than in WT males. This apparent sex-dependent concentrating advantage was absent in Atp6v1b1-/- females, whose reduced AQP2 apical relocation was similar to WT males. Accordingly, female mice concentrate urine better than males upon dehydration due to increased AQP2 expression and mobilization. Moreover, our data support the involvement of ICs in water homeostasis, at least partly mediated by V-ATPase, in a sex-dependent manner.
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PMID:Sex-dependent differences in water homeostasis in wild-type and V-ATPase B1-subunit deficient mice. 3138 75

Norepinephrine (NE) is widely used to treat cardiac arrest and profound hypotension. A prolonged vasoconstriction of blood vessel could cause ischemia and hypoxia which results in a decrease in intracellular pH. V-ATPases pump protons across the plasma membranes of numerous cell types. V-ATPases-mediated intracellular regulation in the ischemic kidney is incompletely studied; we sought to determine the roles of V-ATPases in mice treated with NE causing vasoconstriction or acetylcholine causing vasodilatation to enable comparison of its relative contributions to the affected mice. Mice were divided into 5 groups. Histology and immunohistochemistry were performed to examine pathologic changes in nephron segments. The expression of V-ATPases B1, B2 subunits were examined by Q-PCR and western blotting correlated with the transcription and translation of V-ATPase. All NE treated mice exhibited pronounced renal tubular degradation. However, the tubular pathologies were reversed by ACh. In immunohistochemical studies, NE treated mice showed a higher density of staining in the collecting ducts. These changes were gradually diminished by the treatment with Ach after NE. In Q-PCR, V-ATPase B1 subunit showed a fair expression in all subsets. Western blotting analysis has shown V-ATPase B1 statistical significance in multiple groups treated by NE alone or ACh post to NE. The overdosage of norepinephrine in clinical treatment is harmful to the kidney by vasoconstriction caused hypoxia and acidosis. Our data demonstrated that acetylcholine as a vasodilating agent could aid the cells recovery from hypoxic condition. V-ATPase plays a role by removing H+ allowing cells to recover from cellular acidosis. These findings also help us understand the pathophysiology of renal tubular disorders.
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PMID:Roles of vacuolar H+-ATPase in mice treated with norepinephrine and acetylcholine. 3266 66