Vacuolar H+-ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosis
Aims: Hypercalcaemia is known to be associated with systemic metabolic alkalosis, although the underlying mechanism is uncertain. Therefore, we aimed to examine whether hypercalcaemia was associated with changes in the expression of acid–base transporters in the kidney. Methods: Rats were infused...
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| Veröffentlicht in: | Acta Physiologica 2007-04, Vol.189 (4), p.359-368 |
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| creator | Wang, W. Praetorius, J. Li, C. Praetorius, H. A. Kwon, T.-H. Frøkiær, J. Nielsen, S. |
| description | Aims: Hypercalcaemia is known to be associated with systemic metabolic alkalosis, although the underlying mechanism is uncertain. Therefore, we aimed to examine whether hypercalcaemia was associated with changes in the expression of acid–base transporters in the kidney.
Methods: Rats were infused with human parathyroid hormone (PTH, 15 μg kg−1 day−1), or vehicle for 48 h using osmotic minipumps.
Results: The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 ± 0.8 vs. 28.1 ± 0.8 mmol L−1 in controls, P |
| doi_str_mv | 10.1111/j.1748-1716.2007.01672.x |
| format | Article |
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Methods: Rats were infused with human parathyroid hormone (PTH, 15 μg kg−1 day−1), or vehicle for 48 h using osmotic minipumps.
Results: The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 ± 0.8 vs. 28.1 ± 0.8 mmol L−1 in controls, P < 0.05, n = 6), whereas the urine pH of 6.85 ± 0.1 was significantly decreased compared with the pH of 7.38 ± 0.1 in controls (P < 0.05, n = 12). The observed alkalosis was associated with a significantly increased expression of the B1‐subunit of the H+‐ATPase in kidney inner medulla (IM, 233 ± 45% of the control level). In contrast, electroneutral Na+‐HCO cotransporter NBCn1 and Cl−/HCO anion exchanger AE2 expression was markedly reduced in the inner stripe of the outer medulla (to 26 ± 9% and 65 ± 6%, respectively). These findings were verified by immunohistochemistry.
Conclusions: (1) hypercalcaemia‐induced metabolic alkalosis was associated with increased urinary excretion of H+; (2) the increased H+‐ATPase expression in IM may partly explain the enhanced urinary acidification, which is speculated to prevent stone formation because of hypercalciuria and (3) the decreased expression of outer medullary AE2 suggests a compensatory reduction of the transepithelial bicarbonate transport.</description><identifier>ISSN: 1748-1708</identifier><identifier>EISSN: 1748-1716</identifier><identifier>DOI: 10.1111/j.1748-1716.2007.01672.x</identifier><identifier>PMID: 17367404</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Alkalosis - blood ; Alkalosis - metabolism ; Animals ; Anion Exchange Protein 1, Erythrocyte - analysis ; anion exchanger AE2 ; Anion Transport Proteins - analysis ; Antiporters - analysis ; Biological and medical sciences ; Chloride-Bicarbonate Antiporters - analysis ; electroneutral NBCn1 ; Fundamental and applied biological sciences. Psychology ; H+-ATPase ; Hypercalcemia - blood ; Hypercalcemia - metabolism ; Immunohistochemistry - methods ; Infusions, Parenteral ; kidney ; Kidney - enzymology ; Kidney - metabolism ; Kidney Cortex - enzymology ; Kidney Cortex - metabolism ; Kidney Medulla - enzymology ; Kidney Medulla - metabolism ; Male ; metabolic alkalosis ; Parathyroid Hormone - administration & dosage ; Proton-Translocating ATPases - analysis ; Rats ; Rats, Wistar ; SLC4A Proteins ; Sodium-Bicarbonate Symporters - analysis ; Vacuoles - enzymology ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Acta Physiologica, 2007-04, Vol.189 (4), p.359-368</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4362-4ab9d75a3a9667cf5352d1f17cc02a05bfc879432f2b3b557b4cc6a5a28eea7b3</citedby><cites>FETCH-LOGICAL-c4362-4ab9d75a3a9667cf5352d1f17cc02a05bfc879432f2b3b557b4cc6a5a28eea7b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1748-1716.2007.01672.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1748-1716.2007.01672.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18588747$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17367404$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, W.</creatorcontrib><creatorcontrib>Praetorius, J.</creatorcontrib><creatorcontrib>Li, C.</creatorcontrib><creatorcontrib>Praetorius, H. A.</creatorcontrib><creatorcontrib>Kwon, T.-H.</creatorcontrib><creatorcontrib>Frøkiær, J.</creatorcontrib><creatorcontrib>Nielsen, S.</creatorcontrib><title>Vacuolar H+-ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosis</title><title>Acta Physiologica</title><addtitle>Acta Physiol (Oxf)</addtitle><description>Aims: Hypercalcaemia is known to be associated with systemic metabolic alkalosis, although the underlying mechanism is uncertain. Therefore, we aimed to examine whether hypercalcaemia was associated with changes in the expression of acid–base transporters in the kidney.
Methods: Rats were infused with human parathyroid hormone (PTH, 15 μg kg−1 day−1), or vehicle for 48 h using osmotic minipumps.
Results: The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 ± 0.8 vs. 28.1 ± 0.8 mmol L−1 in controls, P < 0.05, n = 6), whereas the urine pH of 6.85 ± 0.1 was significantly decreased compared with the pH of 7.38 ± 0.1 in controls (P < 0.05, n = 12). The observed alkalosis was associated with a significantly increased expression of the B1‐subunit of the H+‐ATPase in kidney inner medulla (IM, 233 ± 45% of the control level). In contrast, electroneutral Na+‐HCO cotransporter NBCn1 and Cl−/HCO anion exchanger AE2 expression was markedly reduced in the inner stripe of the outer medulla (to 26 ± 9% and 65 ± 6%, respectively). These findings were verified by immunohistochemistry.
Conclusions: (1) hypercalcaemia‐induced metabolic alkalosis was associated with increased urinary excretion of H+; (2) the increased H+‐ATPase expression in IM may partly explain the enhanced urinary acidification, which is speculated to prevent stone formation because of hypercalciuria and (3) the decreased expression of outer medullary AE2 suggests a compensatory reduction of the transepithelial bicarbonate transport.</description><subject>Alkalosis - blood</subject><subject>Alkalosis - metabolism</subject><subject>Animals</subject><subject>Anion Exchange Protein 1, Erythrocyte - analysis</subject><subject>anion exchanger AE2</subject><subject>Anion Transport Proteins - analysis</subject><subject>Antiporters - analysis</subject><subject>Biological and medical sciences</subject><subject>Chloride-Bicarbonate Antiporters - analysis</subject><subject>electroneutral NBCn1</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>H+-ATPase</subject><subject>Hypercalcemia - blood</subject><subject>Hypercalcemia - metabolism</subject><subject>Immunohistochemistry - methods</subject><subject>Infusions, Parenteral</subject><subject>kidney</subject><subject>Kidney - enzymology</subject><subject>Kidney - metabolism</subject><subject>Kidney Cortex - enzymology</subject><subject>Kidney Cortex - metabolism</subject><subject>Kidney Medulla - enzymology</subject><subject>Kidney Medulla - metabolism</subject><subject>Male</subject><subject>metabolic alkalosis</subject><subject>Parathyroid Hormone - administration & dosage</subject><subject>Proton-Translocating ATPases - analysis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>SLC4A Proteins</subject><subject>Sodium-Bicarbonate Symporters - analysis</subject><subject>Vacuoles - enzymology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>1748-1708</issn><issn>1748-1716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u00AQxlcIRKvSV0B7gQuy2X_22hekqIKGKoIiAkhcVuP1mm7i2GHHVpM36GOzbqL0yl52NPObb0bfEEI5S3l871cp16pIuOZ5KhjTKeO5FunuGTk_FZ6fYlackUvEFWOMCy6VEC_JGdcy14qpc_LwE-zYtxDo_F0yW94COup22-AQfd9Rj9R3NriYrmNEwfo6QRczg-_-xMzggoUWhli2rm0nnK593bk90r6hAQak9364o3f77SNqwW08JL6rRxuboF1D26PHV-RFAy26y-N_QX58-ri8mieLr9efr2aLxCqZi0RBVdY6AwllnmvbZDITNW-4tpYJYFnV2EKXSopGVLLKMl0pa3PIQBTOga7kBXl70N2G_u_ocDAbj9Pq0Ll-RKOZ0KWUZQSLA2hDjxhcY7bBbyDsDWdmOoRZmcljM_ltpkOYx0OYXWx9fZwxVhtXPzUebY_AmyMAGD1pAnTW4xNXZEWhlY7chwN371u3_-8FzOx2PpvCKJAcBDwObncSgLA2uZY6M7--XJubhfr9TX1fGiX_AVyItXU</recordid><startdate>200704</startdate><enddate>200704</enddate><creator>Wang, W.</creator><creator>Praetorius, J.</creator><creator>Li, C.</creator><creator>Praetorius, H. A.</creator><creator>Kwon, T.-H.</creator><creator>Frøkiær, J.</creator><creator>Nielsen, S.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200704</creationdate><title>Vacuolar H+-ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosis</title><author>Wang, W. ; Praetorius, J. ; Li, C. ; Praetorius, H. A. ; Kwon, T.-H. ; Frøkiær, J. ; Nielsen, S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4362-4ab9d75a3a9667cf5352d1f17cc02a05bfc879432f2b3b557b4cc6a5a28eea7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Alkalosis - blood</topic><topic>Alkalosis - metabolism</topic><topic>Animals</topic><topic>Anion Exchange Protein 1, Erythrocyte - analysis</topic><topic>anion exchanger AE2</topic><topic>Anion Transport Proteins - analysis</topic><topic>Antiporters - analysis</topic><topic>Biological and medical sciences</topic><topic>Chloride-Bicarbonate Antiporters - analysis</topic><topic>electroneutral NBCn1</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>H+-ATPase</topic><topic>Hypercalcemia - blood</topic><topic>Hypercalcemia - metabolism</topic><topic>Immunohistochemistry - methods</topic><topic>Infusions, Parenteral</topic><topic>kidney</topic><topic>Kidney - enzymology</topic><topic>Kidney - metabolism</topic><topic>Kidney Cortex - enzymology</topic><topic>Kidney Cortex - metabolism</topic><topic>Kidney Medulla - enzymology</topic><topic>Kidney Medulla - metabolism</topic><topic>Male</topic><topic>metabolic alkalosis</topic><topic>Parathyroid Hormone - administration & dosage</topic><topic>Proton-Translocating ATPases - analysis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>SLC4A Proteins</topic><topic>Sodium-Bicarbonate Symporters - analysis</topic><topic>Vacuoles - enzymology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, W.</creatorcontrib><creatorcontrib>Praetorius, J.</creatorcontrib><creatorcontrib>Li, C.</creatorcontrib><creatorcontrib>Praetorius, H. A.</creatorcontrib><creatorcontrib>Kwon, T.-H.</creatorcontrib><creatorcontrib>Frøkiær, J.</creatorcontrib><creatorcontrib>Nielsen, S.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Acta Physiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, W.</au><au>Praetorius, J.</au><au>Li, C.</au><au>Praetorius, H. A.</au><au>Kwon, T.-H.</au><au>Frøkiær, J.</au><au>Nielsen, S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vacuolar H+-ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosis</atitle><jtitle>Acta Physiologica</jtitle><addtitle>Acta Physiol (Oxf)</addtitle><date>2007-04</date><risdate>2007</risdate><volume>189</volume><issue>4</issue><spage>359</spage><epage>368</epage><pages>359-368</pages><issn>1748-1708</issn><eissn>1748-1716</eissn><abstract>Aims: Hypercalcaemia is known to be associated with systemic metabolic alkalosis, although the underlying mechanism is uncertain. Therefore, we aimed to examine whether hypercalcaemia was associated with changes in the expression of acid–base transporters in the kidney.
Methods: Rats were infused with human parathyroid hormone (PTH, 15 μg kg−1 day−1), or vehicle for 48 h using osmotic minipumps.
Results: The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 ± 0.8 vs. 28.1 ± 0.8 mmol L−1 in controls, P < 0.05, n = 6), whereas the urine pH of 6.85 ± 0.1 was significantly decreased compared with the pH of 7.38 ± 0.1 in controls (P < 0.05, n = 12). The observed alkalosis was associated with a significantly increased expression of the B1‐subunit of the H+‐ATPase in kidney inner medulla (IM, 233 ± 45% of the control level). In contrast, electroneutral Na+‐HCO cotransporter NBCn1 and Cl−/HCO anion exchanger AE2 expression was markedly reduced in the inner stripe of the outer medulla (to 26 ± 9% and 65 ± 6%, respectively). These findings were verified by immunohistochemistry.
Conclusions: (1) hypercalcaemia‐induced metabolic alkalosis was associated with increased urinary excretion of H+; (2) the increased H+‐ATPase expression in IM may partly explain the enhanced urinary acidification, which is speculated to prevent stone formation because of hypercalciuria and (3) the decreased expression of outer medullary AE2 suggests a compensatory reduction of the transepithelial bicarbonate transport.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17367404</pmid><doi>10.1111/j.1748-1716.2007.01672.x</doi><tpages>10</tpages></addata></record> |
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| ispartof | Acta Physiologica, 2007-04, Vol.189 (4), p.359-368 |
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| subjects | Alkalosis - blood Alkalosis - metabolism Animals Anion Exchange Protein 1, Erythrocyte - analysis anion exchanger AE2 Anion Transport Proteins - analysis Antiporters - analysis Biological and medical sciences Chloride-Bicarbonate Antiporters - analysis electroneutral NBCn1 Fundamental and applied biological sciences. Psychology H+-ATPase Hypercalcemia - blood Hypercalcemia - metabolism Immunohistochemistry - methods Infusions, Parenteral kidney Kidney - enzymology Kidney - metabolism Kidney Cortex - enzymology Kidney Cortex - metabolism Kidney Medulla - enzymology Kidney Medulla - metabolism Male metabolic alkalosis Parathyroid Hormone - administration & dosage Proton-Translocating ATPases - analysis Rats Rats, Wistar SLC4A Proteins Sodium-Bicarbonate Symporters - analysis Vacuoles - enzymology Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Vacuolar H+-ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosis |
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