Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells
Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells. The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5mM Li was without effect, 10mM, 25mM and 50mM Li significantly decreased...
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Veröffentlicht in: | Kidney international 1990-05, Vol.37 (5), p.1211-1218 |
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description | Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells. The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5mM Li was without effect, 10mM, 25mM and 50mM Li significantly decreased AVP-stimulated cAMP formation. In contrast, cells grown in 5mM Li for 72hours which caused no morphologic changes enhanced cAMP formation (fmol/μg protein) in response to both 10nM AVP (114.5 ± 9.2 vs. 71.6 ± 7.4,P > 0.005) and 100nM AVP (182 ± 14 vs. 120 ± 8.3, P < 0.001), N = 16. A similar enhancement was observed when cAMP formation was stimulated by a post-receptor agonist, cholera toxin. The role of eicosanoids was examined with 5 μM meclofenamate which reversed Li-enhanced cAMP formation in response to both AVP and cholera toxin. To define the eicosanoid responsible, cyclooxygenase products were measured. Prostaglandin E2; and thromboxane B2 synthesis were unchanged by Li, but the production of prostacyclin was significantly (P < 0.02) increased. Prostacyclin (3 μM) mimicked the effect of Li to enhance the response to 10nM AVP as cAMP levels increased from 100 ± 11 to 173 ± 13, P < 0.05. The experiments suggest that acute exposure of Li at concentrations of 10mM or greater inhibit cAMP formation but prolonged Li exposure enhances cAMP formation by increasing the formation of prostacyclin. |
doi_str_mv | 10.1038/ki.1990.104 |
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The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5mM Li was without effect, 10mM, 25mM and 50mM Li significantly decreased AVP-stimulated cAMP formation. In contrast, cells grown in 5mM Li for 72hours which caused no morphologic changes enhanced cAMP formation (fmol/μg protein) in response to both 10nM AVP (114.5 ± 9.2 vs. 71.6 ± 7.4,P > 0.005) and 100nM AVP (182 ± 14 vs. 120 ± 8.3, P < 0.001), N = 16. A similar enhancement was observed when cAMP formation was stimulated by a post-receptor agonist, cholera toxin. The role of eicosanoids was examined with 5 μM meclofenamate which reversed Li-enhanced cAMP formation in response to both AVP and cholera toxin. To define the eicosanoid responsible, cyclooxygenase products were measured. Prostaglandin E2; and thromboxane B2 synthesis were unchanged by Li, but the production of prostacyclin was significantly (P < 0.02) increased. Prostacyclin (3 μM) mimicked the effect of Li to enhance the response to 10nM AVP as cAMP levels increased from 100 ± 11 to 173 ± 13, P < 0.05. The experiments suggest that acute exposure of Li at concentrations of 10mM or greater inhibit cAMP formation but prolonged Li exposure enhances cAMP formation by increasing the formation of prostacyclin.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.1990.104</identifier><identifier>PMID: 2161061</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Arginine Vasopressin - pharmacology ; Biological and medical sciences ; Cells, Cultured ; Cholera Toxin - pharmacology ; Cyclic AMP - biosynthesis ; Drug toxicity and drugs side effects treatment ; Eicosanoids - biosynthesis ; Epoprostenol - pharmacology ; Kidney Medulla - drug effects ; Kidney Medulla - metabolism ; Kidney Tubules - metabolism ; Kidney Tubules, Collecting - drug effects ; Kidney Tubules, Collecting - metabolism ; Lithium - pharmacology ; Meclofenamic Acid - pharmacology ; Medical sciences ; Pharmacology. Drug treatments ; Rats ; Toxicity: urogenital system</subject><ispartof>Kidney international, 1990-05, Vol.37 (5), p.1211-1218</ispartof><rights>1990 International Society of Nephrology</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-6fde2e94973b8f7438dd10ce2b18232ea7aae0c89b6b7a363b637b6e844523bd3</citedby><cites>FETCH-LOGICAL-c421t-6fde2e94973b8f7438dd10ce2b18232ea7aae0c89b6b7a363b637b6e844523bd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19400871$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2161061$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Anger, Michael S.</creatorcontrib><creatorcontrib>Shanley, Paul</creatorcontrib><creatorcontrib>Mansour, Julie</creatorcontrib><creatorcontrib>Berl, Tomas</creatorcontrib><title>Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells. The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5mM Li was without effect, 10mM, 25mM and 50mM Li significantly decreased AVP-stimulated cAMP formation. In contrast, cells grown in 5mM Li for 72hours which caused no morphologic changes enhanced cAMP formation (fmol/μg protein) in response to both 10nM AVP (114.5 ± 9.2 vs. 71.6 ± 7.4,P > 0.005) and 100nM AVP (182 ± 14 vs. 120 ± 8.3, P < 0.001), N = 16. A similar enhancement was observed when cAMP formation was stimulated by a post-receptor agonist, cholera toxin. The role of eicosanoids was examined with 5 μM meclofenamate which reversed Li-enhanced cAMP formation in response to both AVP and cholera toxin. To define the eicosanoid responsible, cyclooxygenase products were measured. Prostaglandin E2; and thromboxane B2 synthesis were unchanged by Li, but the production of prostacyclin was significantly (P < 0.02) increased. Prostacyclin (3 μM) mimicked the effect of Li to enhance the response to 10nM AVP as cAMP levels increased from 100 ± 11 to 173 ± 13, P < 0.05. The experiments suggest that acute exposure of Li at concentrations of 10mM or greater inhibit cAMP formation but prolonged Li exposure enhances cAMP formation by increasing the formation of prostacyclin.</description><subject>Animals</subject><subject>Arginine Vasopressin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Cholera Toxin - pharmacology</subject><subject>Cyclic AMP - biosynthesis</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Eicosanoids - biosynthesis</subject><subject>Epoprostenol - pharmacology</subject><subject>Kidney Medulla - drug effects</subject><subject>Kidney Medulla - metabolism</subject><subject>Kidney Tubules - metabolism</subject><subject>Kidney Tubules, Collecting - drug effects</subject><subject>Kidney Tubules, Collecting - metabolism</subject><subject>Lithium - pharmacology</subject><subject>Meclofenamic Acid - pharmacology</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Toxicity: urogenital system</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkDtPwzAUhS0EKqUwMSO8MKEUO3YSZ6wQL6kIBhhRZDvXxdRNKjtB4t_jKFVZmK7OPZ_u4yB0TsmcEiZu1nZOy3IQ_ABNaZayhBZZdoimhIgsSTMmjtFJCF8k6pKRCZqkNKckp1P0cWcM6C7g1mBnu0_bb3DbYL14fsUraMDLzkZtY6t3Xe-hxrEVdbTwBureOel_sG6di2Nss8Jdr3oHWINz4RQdGekCnO3qDL3f373dPibLl4en28Uy0TylXZKbGlIoeVkwJUzBmahrSjSkioqUpSALKYFoUapcFZLlTOWsUDkIzuOzqmYzdD3O1b4NwYOptt5u4mEVJdWQUbW21ZBRFDzSFyO97VV8Yc_uQon-1c6XQUtnvGy0DX8jSx5zLAbucuQaOSSzB9Z2WDVuykYC4vPfFnwVtIVGQ219jKuqW_vvhb-Zw4vm</recordid><startdate>19900501</startdate><enddate>19900501</enddate><creator>Anger, Michael S.</creator><creator>Shanley, Paul</creator><creator>Mansour, Julie</creator><creator>Berl, Tomas</creator><general>Elsevier Inc</general><general>Nature Publishing</general><scope>6I.</scope><scope>AAFTH</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></search><sort><creationdate>19900501</creationdate><title>Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells</title><author>Anger, Michael S. ; Shanley, Paul ; Mansour, Julie ; Berl, Tomas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-6fde2e94973b8f7438dd10ce2b18232ea7aae0c89b6b7a363b637b6e844523bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Arginine Vasopressin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Cholera Toxin - pharmacology</topic><topic>Cyclic AMP - biosynthesis</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Eicosanoids - biosynthesis</topic><topic>Epoprostenol - pharmacology</topic><topic>Kidney Medulla - drug effects</topic><topic>Kidney Medulla - metabolism</topic><topic>Kidney Tubules - metabolism</topic><topic>Kidney Tubules, Collecting - drug effects</topic><topic>Kidney Tubules, Collecting - metabolism</topic><topic>Lithium - pharmacology</topic><topic>Meclofenamic Acid - pharmacology</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Toxicity: urogenital system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Anger, Michael S.</creatorcontrib><creatorcontrib>Shanley, Paul</creatorcontrib><creatorcontrib>Mansour, Julie</creatorcontrib><creatorcontrib>Berl, Tomas</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Anger, Michael S.</au><au>Shanley, Paul</au><au>Mansour, Julie</au><au>Berl, Tomas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1990-05-01</date><risdate>1990</risdate><volume>37</volume><issue>5</issue><spage>1211</spage><epage>1218</epage><pages>1211-1218</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells. The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5mM Li was without effect, 10mM, 25mM and 50mM Li significantly decreased AVP-stimulated cAMP formation. In contrast, cells grown in 5mM Li for 72hours which caused no morphologic changes enhanced cAMP formation (fmol/μg protein) in response to both 10nM AVP (114.5 ± 9.2 vs. 71.6 ± 7.4,P > 0.005) and 100nM AVP (182 ± 14 vs. 120 ± 8.3, P < 0.001), N = 16. A similar enhancement was observed when cAMP formation was stimulated by a post-receptor agonist, cholera toxin. The role of eicosanoids was examined with 5 μM meclofenamate which reversed Li-enhanced cAMP formation in response to both AVP and cholera toxin. To define the eicosanoid responsible, cyclooxygenase products were measured. Prostaglandin E2; and thromboxane B2 synthesis were unchanged by Li, but the production of prostacyclin was significantly (P < 0.02) increased. Prostacyclin (3 μM) mimicked the effect of Li to enhance the response to 10nM AVP as cAMP levels increased from 100 ± 11 to 173 ± 13, P < 0.05. The experiments suggest that acute exposure of Li at concentrations of 10mM or greater inhibit cAMP formation but prolonged Li exposure enhances cAMP formation by increasing the formation of prostacyclin.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>2161061</pmid><doi>10.1038/ki.1990.104</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arginine Vasopressin - pharmacology Biological and medical sciences Cells, Cultured Cholera Toxin - pharmacology Cyclic AMP - biosynthesis Drug toxicity and drugs side effects treatment Eicosanoids - biosynthesis Epoprostenol - pharmacology Kidney Medulla - drug effects Kidney Medulla - metabolism Kidney Tubules - metabolism Kidney Tubules, Collecting - drug effects Kidney Tubules, Collecting - metabolism Lithium - pharmacology Meclofenamic Acid - pharmacology Medical sciences Pharmacology. Drug treatments Rats Toxicity: urogenital system |
title | Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells |
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