Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells
The mechanism of Ca2+ influx stimulated by arginine vasopressin (AVP) was studied in cultured rat smooth muscle cells. AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the A...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1989-06, Vol.161 (2), p.677-682 |
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| container_title | Biochemical and biophysical research communications |
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| creator | KONDON, K KOZAWA, O TAKATSUKI, K OISO, Y |
| description | The mechanism of Ca2+ influx stimulated by arginine vasopressin (AVP) was studied in cultured rat smooth muscle cells. AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the AVP-stimulated 45Ca2+ influx. The 45Ca2+ influx stimulated by a combination of AVP and NaF was not additive. The affinity of AVP receptor was decreased by guanosine 5'-O-(3-thiotriphosphate). Pertussis toxin failed to affect the AVP-stimulated 45Ca2+ influx. AVP did not stimulate cAMP production, but increased inositol trisphosphate generation. Both AVP-stimulated 45Ca2+ influx and inositol trisphosphate generation were inhibited by neomycin, a phospholipase C inhibitor, in a dose-dependent manner, and the patterns of both inhibitions were similar. These results suggest that, in rat smooth muscle cells, AVP-stimulated Ca2+ influx is mediated exclusively through phosphoinositide hydrolysis. |
| doi_str_mv | 10.1016/0006-291x(89)92652-1 |
| format | Article |
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AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the AVP-stimulated 45Ca2+ influx. The 45Ca2+ influx stimulated by a combination of AVP and NaF was not additive. The affinity of AVP receptor was decreased by guanosine 5'-O-(3-thiotriphosphate). Pertussis toxin failed to affect the AVP-stimulated 45Ca2+ influx. AVP did not stimulate cAMP production, but increased inositol trisphosphate generation. Both AVP-stimulated 45Ca2+ influx and inositol trisphosphate generation were inhibited by neomycin, a phospholipase C inhibitor, in a dose-dependent manner, and the patterns of both inhibitions were similar. These results suggest that, in rat smooth muscle cells, AVP-stimulated Ca2+ influx is mediated exclusively through phosphoinositide hydrolysis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/0006-291x(89)92652-1</identifier><identifier>PMID: 2544169</identifier><identifier>CODEN: BBRCA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier</publisher><subject>Aminoacids, peptides. Hormones. Neuropeptides ; Analytical, structural and metabolic biochemistry ; Animals ; Arginine Vasopressin - pharmacology ; Biological and medical sciences ; Calcium - metabolism ; Cell Membrane - metabolism ; Cyclic AMP - metabolism ; Fluorides - pharmacology ; Fundamental and applied biological sciences. Psychology ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Triphosphate - analogs & derivatives ; Guanosine Triphosphate - pharmacology ; In Vitro Techniques ; Inositol Phosphates - metabolism ; Muscle, Smooth, Vascular - metabolism ; Neomycin - pharmacology ; Pertussis Toxin ; Phosphatidylinositols - metabolism ; Proteins ; Rats ; Rats, Inbred Strains ; Receptors, Angiotensin - metabolism ; Receptors, Vasopressin ; Sugar Phosphates - metabolism ; Thionucleotides - pharmacology ; Virulence Factors, Bordetella - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 1989-06, Vol.161 (2), p.677-682</ispartof><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2449-28027be784b54fbfa7da9ac1001dc50ce9691c4319498173648d7f765748f92d3</citedby><cites>FETCH-LOGICAL-c2449-28027be784b54fbfa7da9ac1001dc50ce9691c4319498173648d7f765748f92d3</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=7291923$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2544169$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KONDON, K</creatorcontrib><creatorcontrib>KOZAWA, O</creatorcontrib><creatorcontrib>TAKATSUKI, K</creatorcontrib><creatorcontrib>OISO, Y</creatorcontrib><title>Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The mechanism of Ca2+ influx stimulated by arginine vasopressin (AVP) was studied in cultured rat smooth muscle cells. AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the AVP-stimulated 45Ca2+ influx. The 45Ca2+ influx stimulated by a combination of AVP and NaF was not additive. The affinity of AVP receptor was decreased by guanosine 5'-O-(3-thiotriphosphate). Pertussis toxin failed to affect the AVP-stimulated 45Ca2+ influx. AVP did not stimulate cAMP production, but increased inositol trisphosphate generation. Both AVP-stimulated 45Ca2+ influx and inositol trisphosphate generation were inhibited by neomycin, a phospholipase C inhibitor, in a dose-dependent manner, and the patterns of both inhibitions were similar. These results suggest that, in rat smooth muscle cells, AVP-stimulated Ca2+ influx is mediated exclusively through phosphoinositide hydrolysis.</description><subject>Aminoacids, peptides. Hormones. Neuropeptides</subject><subject>Analytical, structural and metabolic biochemistry</subject><subject>Animals</subject><subject>Arginine Vasopressin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>Cell Membrane - metabolism</subject><subject>Cyclic AMP - metabolism</subject><subject>Fluorides - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guanosine 5'-O-(3-Thiotriphosphate)</subject><subject>Guanosine Triphosphate - analogs & derivatives</subject><subject>Guanosine Triphosphate - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Inositol Phosphates - metabolism</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Neomycin - pharmacology</subject><subject>Pertussis Toxin</subject><subject>Phosphatidylinositols - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Receptors, Angiotensin - metabolism</subject><subject>Receptors, Vasopressin</subject><subject>Sugar Phosphates - metabolism</subject><subject>Thionucleotides - pharmacology</subject><subject>Virulence Factors, Bordetella - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1r3DAQhkVp2WzS_oMGdCghobjVyLJkHcOSj0IglxR6E7Iss2psa6Oxy-6_j7bZzWGYw_vMy_AQ8hXYD2AgfzLGZME1bC9rfaW5rHgBH8gSmGYFByY-kuUR-XNCThH_MgYgpF6QBa-EAKmX5Hll-Xcaxq6ftxSnMMy9nXxLmx39ZzFukkcMIw1IB9-GY7RZR8wTxohhCq2n612bYr_DzGU62YniEOO0psOMrvfU-b7Hz-RTZ3v0Xw77jPy-vXla3RcPj3e_VtcPheNC6ILXjKvGq1o0leiazqrWausgf9-6ijmvpQYnStBC16BKKepWdUpWStSd5m15Ri7eejcpvsweJzME3H9gRx9nNEqzEhSTGRRvoEsRMfnObFIYbNoZYGbv2OwFmr1AU2vz37GBfHZ-6J-bbOX96CA1598OuUVn-y7Z0QV8x1Tu07wsXwGqQoUb</recordid><startdate>19890615</startdate><enddate>19890615</enddate><creator>KONDON, K</creator><creator>KOZAWA, O</creator><creator>TAKATSUKI, K</creator><creator>OISO, Y</creator><general>Elsevier</general><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>19890615</creationdate><title>Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells</title><author>KONDON, K ; KOZAWA, O ; TAKATSUKI, K ; OISO, Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2449-28027be784b54fbfa7da9ac1001dc50ce9691c4319498173648d7f765748f92d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Aminoacids, peptides. Hormones. Neuropeptides</topic><topic>Analytical, structural and metabolic biochemistry</topic><topic>Animals</topic><topic>Arginine Vasopressin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>Cell Membrane - metabolism</topic><topic>Cyclic AMP - metabolism</topic><topic>Fluorides - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guanosine 5'-O-(3-Thiotriphosphate)</topic><topic>Guanosine Triphosphate - analogs & derivatives</topic><topic>Guanosine Triphosphate - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Inositol Phosphates - metabolism</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Neomycin - pharmacology</topic><topic>Pertussis Toxin</topic><topic>Phosphatidylinositols - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Receptors, Angiotensin - metabolism</topic><topic>Receptors, Vasopressin</topic><topic>Sugar Phosphates - metabolism</topic><topic>Thionucleotides - pharmacology</topic><topic>Virulence Factors, Bordetella - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KONDON, K</creatorcontrib><creatorcontrib>KOZAWA, O</creatorcontrib><creatorcontrib>TAKATSUKI, K</creatorcontrib><creatorcontrib>OISO, Y</creatorcontrib><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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KONDON, K</au><au>KOZAWA, O</au><au>TAKATSUKI, K</au><au>OISO, Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1989-06-15</date><risdate>1989</risdate><volume>161</volume><issue>2</issue><spage>677</spage><epage>682</epage><pages>677-682</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><coden>BBRCA9</coden><abstract>The mechanism of Ca2+ influx stimulated by arginine vasopressin (AVP) was studied in cultured rat smooth muscle cells. AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the AVP-stimulated 45Ca2+ influx. The 45Ca2+ influx stimulated by a combination of AVP and NaF was not additive. The affinity of AVP receptor was decreased by guanosine 5'-O-(3-thiotriphosphate). Pertussis toxin failed to affect the AVP-stimulated 45Ca2+ influx. AVP did not stimulate cAMP production, but increased inositol trisphosphate generation. Both AVP-stimulated 45Ca2+ influx and inositol trisphosphate generation were inhibited by neomycin, a phospholipase C inhibitor, in a dose-dependent manner, and the patterns of both inhibitions were similar. These results suggest that, in rat smooth muscle cells, AVP-stimulated Ca2+ influx is mediated exclusively through phosphoinositide hydrolysis.</abstract><cop>San Diego, CA</cop><pub>Elsevier</pub><pmid>2544169</pmid><doi>10.1016/0006-291x(89)92652-1</doi><tpages>6</tpages></addata></record> |
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| subjects | Aminoacids, peptides. Hormones. Neuropeptides Analytical, structural and metabolic biochemistry Animals Arginine Vasopressin - pharmacology Biological and medical sciences Calcium - metabolism Cell Membrane - metabolism Cyclic AMP - metabolism Fluorides - pharmacology Fundamental and applied biological sciences. Psychology Guanosine 5'-O-(3-Thiotriphosphate) Guanosine Triphosphate - analogs & derivatives Guanosine Triphosphate - pharmacology In Vitro Techniques Inositol Phosphates - metabolism Muscle, Smooth, Vascular - metabolism Neomycin - pharmacology Pertussis Toxin Phosphatidylinositols - metabolism Proteins Rats Rats, Inbred Strains Receptors, Angiotensin - metabolism Receptors, Vasopressin Sugar Phosphates - metabolism Thionucleotides - pharmacology Virulence Factors, Bordetella - pharmacology |
| title | Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells |
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