Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin and vasopressin antagonists are finding expanded use in mouse models of disease and in clinical medicine. To provide further insight into the physiological role of V1a and V2 vasopressin receptors in the human and mouse kidney, intrarenal localization of the receptors mRNA was determined by in situ hybridization. V2-receptor mRNA was predominantly expressed in the medulla, whereas mRNA for V1a receptors predominated in the cortex. The segmental localization of vasopressin-receptor mRNAs was determined using simultaneous in situ hybridization and immunohistochemistry for segment-specific markers, including aquaporin-2, Dolichos biflorus agglutinin, epithelial Na channels, Tamm Horsfall glycoprotein, and thiazide-sensitive Na(+)-Cl(-) cotransporter. Notably, V1a receptor expression was exclusively expressed in V-ATPase/anion exchanger-1-labeled alpha-intercalated cells of the medullary collecting duct in both mouse and human kidney. In cortical collecting ducts, V1a mRNA was more widespread and detected in both principal and intercalated cells. V2-receptor mRNA is diffusely expressed along the collecting ducts in both mouse and human kidney, with higher expression levels in the medulla. These results demonstrate heterogenous axial expression of both V1a and V2 vasopressin receptors along the human and mouse collecting duct. The restricted expression of V1a-receptor mRNA in intercalated cells suggests a role for this receptor in acid-base balance. These findings further suggest distinct regulation of renal transport function by AVP through V1a and V2 receptors in the cortex vs. the medulla.
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PMID:Axial heterogeneity of vasopressin-receptor subtypes along the human and mouse collecting duct. 1683 8

Despite early reports, dating back three quarters of a century, of high total CO(2) concentrations in the intestinal fluids of marine teleost fishes, only the past decade has provided some insight into the functional significance of this phenomenon. It is now being recognized that intestinal anion exchange is responsible for high luminal HCO(3)(-) and CO(3)(2-) concentrations while at the same time contributing substantially to intestinal Cl(-) and thereby water absorption, which is vital for marine fish osmoregulation. In species examined to date, the majority of HCO(3)(-) secreted by the apical anion exchange process is derived from hydration of metabolic CO(2) with the resulting H(+) being extruded via a Na(+):H(+) exchange mechanism in the basolateral membrane. The basolateral H(+) extrusion is critical for the apical anion exchange and relies on the Na(+) gradient established by the Na(+)-K(+)-ATPase. This enzyme thereby ultimately fuels the secondary active transport of HCO(3)(-) and Cl(-) by the apical anion exchanger. High cellular HCO(3)(-) concentrations (>10 mmol l(-1)) are required for the anion exchange process and could be the result of both a high metabolic activity of the intestinal epithelium and a close association of the anion exchange protein and the enzyme carbonic anhydrase. The anion exchange activity in vivo is likely most pronounced in the anterior segment and results in net intestinal acid absorption. In contrast to other water absorbing vertebrate epithelia, the marine teleost intestine absorbs what appears to be a hypertonic fluid to displace diffusive fluid loss to the marine environment.
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PMID:Intestinal anion exchange in marine fish osmoregulation. 1685 65

Kidneys are essential for acid-base homeostasis, especially when organisms cope with changes in acid or base dietary intake. Because collecting ducts constitute the final site for regulating urine acid-base balance, we undertook to identify the gene network involved in acid-base transport and regulation in the mouse outer medullary collecting duct (OMCD). For this purpose, we combined kidney functional studies and quantitative analysis of gene expression in OMCDs, by transcriptome and candidate gene approaches, during metabolic acidosis. Furthermore, to better delineate the set of genes concerned with acid-base disturbance, the OMCD transcriptome of acidotic mice was compared with that of both normal mice and mice undergoing an adaptative response through potassium depletion. Metabolic acidosis, achieved through an NH4Cl-supplemented diet for 3 days, not only induced acid secretion but also stimulated the aldosterone and vasopressin systems and triggered cell proliferation. Accordingly, metabolic acidosis increased the expression of genes involved in acid-base transport, sodium transport, water transport, and cell proliferation. In particular, >25 transcripts encoding proteins involved in urine acidification (subunits of H-ATPase, kidney anion exchanger, chloride channel Clcka, carbonic anhydrase-2, aldolase) were co-regulated during acidosis. These transcripts, which cooperate to achieve a similar function and are co-regulated during acidosis, constitute a functional unit that we propose to call a "regulon".
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PMID:Kidney collecting duct acid-base "regulon". 1686 73

Despite all the efforts and technological advances during the last few decades, the cellular mechanisms for branchial chloride uptake in freshwater (FW) fish are still unclear. Although a tight 1 : 1 link with HCO-3 secretion has been established, not much is known about the identity of the ion-transporting proteins involved or the energizing steps that allow for the inward transport of Cl- against the concentration gradient. We propose a new model for Cl- uptake in FW fish whereby the combined action of an apical anion exchanger, cytoplasmic carbonic anhydrase, and basolateral V-type H+ -ATPase creates a local [HCO-3] high enough to energize Cl- uptake. Our model is based on analyses of structure-function relationships, reinterpretation of previous results, and novel observations about gill cell subtypes and immunolocalization of the V-H+ -ATPase.
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PMID:Chloride uptake and base secretion in freshwater fish: a transepithelial ion-transport metabolon? 1704 64

The renal collecting system (CS) is composed of segment-specific (SS) and intercalated (IC) cells. The latter comprise at least two subtypes (type A and non-type A IC). The origin and maintenance of cellular heterogeneity in the CS is unclear. Among other hypotheses, it was proposed that one subtype of IC cells represents a stem cell population from which all cell types in the CS may arise. In the present study, we tested this stem cell hypothesis for the adult kidney by assessing DNA synthesis as a marker for cell replication. SS and IC cells were identified by their characteristic expressions of sodium- (epithelial sodium channel, Na-K-ATPase), water- (aquaporin-2) and acid/base- (H+ -ATPase, anion exchanger AE1) transporting proteins. Immunostaining for bromodeoxyuridine (BrdU) and for the proliferating cell nuclear antigen (PCNA) was used to reveal DNA synthesis in CS epithelium. BrdU- and PCNA-immunostaining as well as mitotic figures were seen in all subtypes of CS cells. Dividing cells retained the cell-type specific expression of marker molecules. Treatment of mice with bumetanide combined with a high oral salt intake, which increases the tubular salt load in the CS, profoundly increased the DNA-synthesis rate in SS and non-type A IC cells, but reduced it in type A IC cells. Thus, our data show that DNA synthesis and cell replication occur in each cell lineage of the CS and in differentiated cells. The replication rate in each cell type can be differently modulated by functional stimulation. Independent proliferation of each cell lineage might contribute to maintain the cellular heterogeneity of the CS of the adult kidney and may also add to the adaptation of the CS to altered functional requirements.
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PMID:Replication of segment-specific and intercalated cells in the mouse renal collecting system. 1718 65

Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H+ secretion and/or HCO3- reabsorption. To identify the molecular mechanisms of these defects, protein expression of key acid-base transporters were examined along the renal nephron and collecting duct of kidneys from rats subjected to 24-h bilateral ureteral obstruction (BUO), 4 days after release of BUO (BUO-R), or BUO-R rats with experimentally induced metabolic acidosis (BUO-A). Semiquantitative immunoblotting revealed that BUO caused a significant reduction in the expression of the type 3 Na+/H+ exchanger (NHE3) in the cortex (21 +/- 4%), electrogenic Na+/HCO3- cotransporter (NBC1; 71 +/- 5%), type 1 bumetanide-sensitive Na+-K+-2Cl- cotransporter (NKCC2; 3 +/- 1%), electroneutral Na+/HCO3- cotransporter (NBCn1; 46 +/- 7%), and anion exchanger (pendrin; 87 +/- 2%). The expression of H+-ATPase increased in the inner medullary collecting duct (152 +/- 13%). These changes were confirmed by immunocytochemistry. In BUO-R rats, there was a persistent downregulation of all the acid-base transporters including H+-ATPase. Two days of NH4Cl loading reduced plasma pH and HCO3- levels in BUO-A rats. The results demonstrate that the expression of multiple renal acid-base transporters are markedly altered in response to BUO, which may be responsible for development of metabolic acidosis and contribute to the urinary acidification defect after release of the obstruction.
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PMID:Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney. 1850 79

Water and solute transport in the efferent ducts and epididymis are important for the establishment of the appropriate luminal environment for sperm maturation and storage. Aquaporin 9 (AQP9) is the main water channel in the epididymis, but its regulation is still poorly understood. Components of the kinin-kallikrein system (KKS), leading to the production of bradykinin (BK), are highly expressed in the lumen of the male reproductive tract. We report here that the epididymal luminal fluid contains a significant amount of BK (2 nM). RT-PCR performed on epididymal epithelial cells isolated by laser capture microdissection (LCM) showed abundant BK type 2 receptor (Bdkrb2) mRNA expression but no type 1 receptor (Bdkrb1). Double-immunofluorescence staining for BDKRB2 and the anion exchanger AE2 (a marker of efferent duct ciliated cells) or the V-ATPase E subunit, official symbol ATP6V1E1 (a marker of epididymal clear cells), showed that BDKRB2 is expressed in the apical pole of nonciliated cells (efferent ducts) and principal cells (epididymis). Triple labeling for BDKRB2, AQP9, and ATP6V1E1 showed that BDKRB2 and AQP9 colocalize in the apical stereocilia of principal cells in the cauda epididymidis. While uniform Bdkrb2 mRNA expression was detected in the efferent ducts and along the epididymal tubule, marked variations were detected at the protein level. BDKRB2 was highest in the efferent ducts and cauda epididymidis, intermediate in the distal initial segment, moderate in the corpus, and undetectable in the proximal initial segment and the caput. Functional assays on tubules isolated from the distal initial segments showed that BK significantly increased AQP9-dependent glycerol apical membrane permeability. This effect was inhibited by BAPTA-AM, demonstrating the participation of calcium in this process. This study, therefore, identifies BK as an important regulator of AQP9.
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PMID:Segmental expression of the bradykinin type 2 receptor in rat efferent ducts and epididymis and its role in the regulation of aquaporin 9. 1882 5

Exposure of trout hepatocytes to hypertonicity induced a decrease in acridine orange (AO) fluorescence, indicating a corresponding decrease in pH inside the lumen of acidic compartments (pH(L)). Pre-exposure of cells to the specific V-ATPase inhibitor bafilomycin A1 (0.3 micromol l(-1)) increased AO fluorescence - unmasking H(+) leaks under steady-state conditions - and partially removed the hypertonicity-induced pH(L) decrease. The sustainability of the luminal acidification, but not the acidification itself, appeared to depend on a low K(+) and a high Cl(-) conductance under hypertonic conditions. Increasing K(+) conductance using the specific ionophore valinomycin (10 micromol l(-1)) or removal of extracellular Cl(-) after an instant drop in AO fluorescence resulted in a reversal of luminal acidity. The alkalinization measured under hypertonic conditions in the absence of Cl(-) was largely attenuated when cells were bathed in HCO(3)(-)-free medium, signifying the possible presence of Cl(-)/HCO(3)(-) exchange. Under steady-state conditions, while a slight and brief pH(L) increase was measured upon exposure of cells to valinomycin, Cl(-) removal, unexpectedly, induced a decrease in pH(L), indicating a role for extracellular Cl(-) in limiting luminal acidification. This was confirmed by the substantial pH(L) decrease measured upon exposure of cells to the anion exchanger inhibitor SITS (0.5 mmol l(-1)). Furthermore, hypertonicity-induced acidification was still noticeable in the presence of SITS. On the other hand, the hypertonicity-induced acidification was significantly reduced in the absence of extracellular Na(+) or Ca(2+). However, BAPTA-AM induced an increase in steady-state pH(L) that was independent of V-ATPase inhibition. Moreover, the BAPTA-induced alkalinization was still apparent after depletion of intracellular Ca(2+) using the Ca(2+) ionophore A23187 in Ca(2+)-free medium. We conclude that pH(L) of trout hepatocytes is sensitive to hypertonicity and ionic determinants of hypertonicity. Thus, changes in pH(L) should be considered when studying pH adaptations to hypertonic stress.
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PMID:Ionic determinants of pH of acidic compartments under hypertonic conditions in trout hepatocytes. 1884 Jun 65

A method is described for the determination by solid phase spectrophotometry (SPS) of trace amounts of vanadium in natural water and crude petroleum samples. The procedure is based on fixation on a dextran-type anion exchanger of the complex V(IV)-Eriochrome Cyanine R. The absorbance of the gel, at 563 and 750 nm, packed in a 1 mm cell, is measured directly. Vanadium can be determined in the 0.6-25.0 mug l(-1) range with a relative standard deviation of 2.2%. The comparison of the SPS method and the gallic acid persulphate method shows that the linearity, analytical sensitivity and precision were better for the SPS method, and that the latter method has lower detection and quantification limits than the gallic acid persulphate method.
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PMID:Determination of vanadium by solid-phase spectrophotometry after its preconcentration as an Eriochrome Cyanine R complex on a dextran-type exchanger. 1896 85

The renal collecting system serves the fine-tuning of renal acid-base secretion. Acid-secretory type-A intercalated cells secrete protons via a luminally expressed V-type H(+)-ATPase and generate new bicarbonate released by basolateral chloride/bicarbonate exchangers including the AE1 anion exchanger. Efficient proton secretion depends both on the presence of titratable acids (mainly phosphate) and the concomitant secretion of ammonia being titrated to ammonium. Collecting duct ammonium excretion requires the Rhesus protein RhCG as indicated by recent KO studies. Urinary acid secretion by type-A intercalated cells is strongly regulated by various factors among them acid-base status, angiotensin II and aldosterone, and the Calcium-sensing receptor. Moreover, urinary acidification by H(+)-ATPases is modulated indirectly by the activity of the epithelial sodium channel ENaC. Bicarbonate secretion is achieved by non-type-A intercalated cells characterized by the luminal expression of the chloride/bicarbonate exchanger pendrin. Pendrin activity is driven by H(+)-ATPases and may serve both bicarbonate excretion and chloride reabsorption. The activity and expression of pendrin is regulated by different factors including acid-base status, chloride delivery, and angiotensin II and may play a role in NaCl retention and blood pressure regulation. Finally, the relative abundance of type-A and non-type-A intercalated cells may be tightly regulated. Dysregulation of intercalated cell function or abundance causes various syndromes of distal renal tubular acidosis underlining the importance of these processes for acid-base homeostasis.
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PMID:Regulated acid-base transport in the collecting duct. 1927


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