Monocytes From Spontaneously Hypertensive Rats Show Increased Store-Operated and Second Messenger-Operated Calcium Influx Mediated by Transient Receptor Potential Canonical Type 3 Channels
We recently showed that increased expression of the transient receptor potential canonical Type 3 (TRPC3) channel is associated with genetic hypertension. It is unknown whether store-operated TRPC3 channels, which are activated after depletion of intracellular stores, or second messenger-operated TR...
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| Veröffentlicht in: | American journal of hypertension 2007-10, Vol.20 (10), p.1111-1118 |
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| creator | Liu, Dao Yan Scholze, Alexandra Kreutz, Reinhold Wehland-von-Trebra, Markus Zidek, Walter Zhu, Zhi Ming Tepel, Martin |
| description | We recently showed that increased expression of the transient receptor potential canonical Type 3 (TRPC3) channel is associated with genetic hypertension. It is unknown whether store-operated TRPC3 channels, which are activated after depletion of intracellular stores, or second messenger-operated TRPC3 channels, which are activated by 1-oleoyl-2-acetyl-sn-glycerol, show augmented responses in monocytes in genetic hypertension and support the development of vascular disease.
Using the fluorescent-dye technique, we studied store-depleted and thapsigargin-induced, store-operated calcium influx and 1-oleoyl-2-acetyl-sn-glycerol-induced second messenger-operated calcium influx into monocytes from spontaneously hypertensive rats (SHRs) and from normotensive Wistar-Kyoto rats (WKYs). The RNA interference for the downregulation of TRPC3 in monocytes by small, interfering RNA (siRNA) was performed and evaluated using in-cell Western assay.
Thapsigargin-induced, store-operated calcium influx was significantly elevated in SHRs and was approximately double that observed in WKYs. In the presence of nimodipine, the thapsigargin-induced, store-operated calcium influx was also significantly higher in SHRs compared with WKYs. After stimulation of monocytes by angiotensin II, calcium influx was significantly elevated in SHRs, and was approximately double that observed in WKYs. The 1-oleoyl-2-acetyl-sn-glycerol-induced, second messenger-operated calcium influx was also significantly elevated in SHRs compared with WKYs. Thapsigargin-induced, store-operated calcium influx was reduced by the inhibitor 2-aminoethoxydiphenyl borane. After TRPC3 knockdown, the thapsigargin-induced, store-operated calcium influx, as well as 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, was significantly more reduced in cells from SHRs compared with WKYs.
The increased store-operated and second messenger-operated calcium influx through TRPC3 channels in monocytes from SHRs may be responsible for a more aggressive effect in promoting vascular disease in genetic hypertension. |
| doi_str_mv | 10.1016/j.amjhyper.2007.04.004 |
| format | Article |
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Using the fluorescent-dye technique, we studied store-depleted and thapsigargin-induced, store-operated calcium influx and 1-oleoyl-2-acetyl-sn-glycerol-induced second messenger-operated calcium influx into monocytes from spontaneously hypertensive rats (SHRs) and from normotensive Wistar-Kyoto rats (WKYs). The RNA interference for the downregulation of TRPC3 in monocytes by small, interfering RNA (siRNA) was performed and evaluated using in-cell Western assay.
Thapsigargin-induced, store-operated calcium influx was significantly elevated in SHRs and was approximately double that observed in WKYs. In the presence of nimodipine, the thapsigargin-induced, store-operated calcium influx was also significantly higher in SHRs compared with WKYs. After stimulation of monocytes by angiotensin II, calcium influx was significantly elevated in SHRs, and was approximately double that observed in WKYs. The 1-oleoyl-2-acetyl-sn-glycerol-induced, second messenger-operated calcium influx was also significantly elevated in SHRs compared with WKYs. Thapsigargin-induced, store-operated calcium influx was reduced by the inhibitor 2-aminoethoxydiphenyl borane. After TRPC3 knockdown, the thapsigargin-induced, store-operated calcium influx, as well as 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, was significantly more reduced in cells from SHRs compared with WKYs.
The increased store-operated and second messenger-operated calcium influx through TRPC3 channels in monocytes from SHRs may be responsible for a more aggressive effect in promoting vascular disease in genetic hypertension.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/j.amjhyper.2007.04.004</identifier><identifier>PMID: 17903696</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; calcium ; Calcium - metabolism ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Diglycerides - pharmacology ; Down-Regulation - drug effects ; Down-Regulation - physiology ; Enzyme Inhibitors - pharmacology ; Experimental diseases ; hypertension ; Hypertension - genetics ; Hypertension - metabolism ; Male ; Medical sciences ; Monocytes ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; RNA, Small Interfering - pharmacology ; Second Messenger Systems - drug effects ; Second Messenger Systems - physiology ; Thapsigargin - pharmacology ; Transient receptor potential canonical Type 3 channel ; TRPC Cation Channels - genetics ; TRPC Cation Channels - metabolism</subject><ispartof>American journal of hypertension, 2007-10, Vol.20 (10), p.1111-1118</ispartof><rights>2007 American Journal of Hypertension, Ltd.</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Oct 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-dc4fd9e440deae6e6c326d6dcc66f081de7088b447b62daa9ae79bd4dccbcb473</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19163536$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17903696$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Dao Yan</creatorcontrib><creatorcontrib>Scholze, Alexandra</creatorcontrib><creatorcontrib>Kreutz, Reinhold</creatorcontrib><creatorcontrib>Wehland-von-Trebra, Markus</creatorcontrib><creatorcontrib>Zidek, Walter</creatorcontrib><creatorcontrib>Zhu, Zhi Ming</creatorcontrib><creatorcontrib>Tepel, Martin</creatorcontrib><title>Monocytes From Spontaneously Hypertensive Rats Show Increased Store-Operated and Second Messenger-Operated Calcium Influx Mediated by Transient Receptor Potential Canonical Type 3 Channels</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>We recently showed that increased expression of the transient receptor potential canonical Type 3 (TRPC3) channel is associated with genetic hypertension. It is unknown whether store-operated TRPC3 channels, which are activated after depletion of intracellular stores, or second messenger-operated TRPC3 channels, which are activated by 1-oleoyl-2-acetyl-sn-glycerol, show augmented responses in monocytes in genetic hypertension and support the development of vascular disease.
Using the fluorescent-dye technique, we studied store-depleted and thapsigargin-induced, store-operated calcium influx and 1-oleoyl-2-acetyl-sn-glycerol-induced second messenger-operated calcium influx into monocytes from spontaneously hypertensive rats (SHRs) and from normotensive Wistar-Kyoto rats (WKYs). The RNA interference for the downregulation of TRPC3 in monocytes by small, interfering RNA (siRNA) was performed and evaluated using in-cell Western assay.
Thapsigargin-induced, store-operated calcium influx was significantly elevated in SHRs and was approximately double that observed in WKYs. In the presence of nimodipine, the thapsigargin-induced, store-operated calcium influx was also significantly higher in SHRs compared with WKYs. After stimulation of monocytes by angiotensin II, calcium influx was significantly elevated in SHRs, and was approximately double that observed in WKYs. The 1-oleoyl-2-acetyl-sn-glycerol-induced, second messenger-operated calcium influx was also significantly elevated in SHRs compared with WKYs. Thapsigargin-induced, store-operated calcium influx was reduced by the inhibitor 2-aminoethoxydiphenyl borane. After TRPC3 knockdown, the thapsigargin-induced, store-operated calcium influx, as well as 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, was significantly more reduced in cells from SHRs compared with WKYs.
The increased store-operated and second messenger-operated calcium influx through TRPC3 channels in monocytes from SHRs may be responsible for a more aggressive effect in promoting vascular disease in genetic hypertension.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>calcium</subject><subject>Calcium - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Diglycerides - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Experimental diseases</subject><subject>hypertension</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monocytes</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Second Messenger Systems - drug effects</subject><subject>Second Messenger Systems - physiology</subject><subject>Thapsigargin - pharmacology</subject><subject>Transient receptor potential canonical Type 3 channel</subject><subject>TRPC Cation Channels - genetics</subject><subject>TRPC Cation Channels - metabolism</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkd9u0zAUxiMEYmPwCpMlBHcpduLYyR2oYnTSpqG1SBM3lmOf0JTU7mxnrO_Gw3FKC5W44erY5_zOH31flp0zOmGUiXeriV6vltsNhElBqZxQPqGUP8lOWS2bnDW0epqd0rqpckkFO8lexLiiSAjBnmcnTDa0FI04zX5ee-fNNkEkF8GvyXzjXdIO_BiHLZntFiRwsX8AcqtTJPOl_0EunQmgI1gyTz5AfoOUTvjVDlNgPIZriBHcNwjH6lQPph_X2N4N4yMStv-db7dkETQuAZfILRjY4FTy2ePi1OsB-5x3vcHXAu8hJZkutXMwxJfZs04PEV4d4ln25eLjYjrLr24-XU4_XOWGiyLl1vDONsA5taBBgDBlIaywxgjR0ZpZkLSuW85lKwqrdaNBNq3lCLSm5bI8y97u526Cvx8hJrXuo4Fh2AulRF2WjDcVgq__AVd-DA5vU4wWleQ1lQVSYk-Z4GMM0KlN6Nc6bBFSO3fVSv1xV-3cVZQr9A4bzw_jx3YN9th2sBOBNwdAR9SrQ1VNH49cw0RZlTsu33N9TPD4t67DdyVkKSs1u_uq5JSxgtWFukP-_Z5H0eGhx7OiQbcMOhjAJGV9_7_bfwEV0tp4</recordid><startdate>20071001</startdate><enddate>20071001</enddate><creator>Liu, Dao Yan</creator><creator>Scholze, Alexandra</creator><creator>Kreutz, Reinhold</creator><creator>Wehland-von-Trebra, Markus</creator><creator>Zidek, Walter</creator><creator>Zhu, Zhi Ming</creator><creator>Tepel, Martin</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20071001</creationdate><title>Monocytes From Spontaneously Hypertensive Rats Show Increased Store-Operated and Second Messenger-Operated Calcium Influx Mediated by Transient Receptor Potential Canonical Type 3 Channels</title><author>Liu, Dao Yan ; Scholze, Alexandra ; Kreutz, Reinhold ; Wehland-von-Trebra, Markus ; Zidek, Walter ; Zhu, Zhi Ming ; Tepel, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-dc4fd9e440deae6e6c326d6dcc66f081de7088b447b62daa9ae79bd4dccbcb473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>calcium</topic><topic>Calcium - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Diglycerides - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Down-Regulation - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Experimental diseases</topic><topic>hypertension</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monocytes</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Second Messenger Systems - drug effects</topic><topic>Second Messenger Systems - physiology</topic><topic>Thapsigargin - pharmacology</topic><topic>Transient receptor potential canonical Type 3 channel</topic><topic>TRPC Cation Channels - genetics</topic><topic>TRPC Cation Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Dao Yan</creatorcontrib><creatorcontrib>Scholze, Alexandra</creatorcontrib><creatorcontrib>Kreutz, Reinhold</creatorcontrib><creatorcontrib>Wehland-von-Trebra, Markus</creatorcontrib><creatorcontrib>Zidek, Walter</creatorcontrib><creatorcontrib>Zhu, Zhi Ming</creatorcontrib><creatorcontrib>Tepel, Martin</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>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Dao Yan</au><au>Scholze, Alexandra</au><au>Kreutz, Reinhold</au><au>Wehland-von-Trebra, Markus</au><au>Zidek, Walter</au><au>Zhu, Zhi Ming</au><au>Tepel, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monocytes From Spontaneously Hypertensive Rats Show Increased Store-Operated and Second Messenger-Operated Calcium Influx Mediated by Transient Receptor Potential Canonical Type 3 Channels</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2007-10-01</date><risdate>2007</risdate><volume>20</volume><issue>10</issue><spage>1111</spage><epage>1118</epage><pages>1111-1118</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>We recently showed that increased expression of the transient receptor potential canonical Type 3 (TRPC3) channel is associated with genetic hypertension. It is unknown whether store-operated TRPC3 channels, which are activated after depletion of intracellular stores, or second messenger-operated TRPC3 channels, which are activated by 1-oleoyl-2-acetyl-sn-glycerol, show augmented responses in monocytes in genetic hypertension and support the development of vascular disease.
Using the fluorescent-dye technique, we studied store-depleted and thapsigargin-induced, store-operated calcium influx and 1-oleoyl-2-acetyl-sn-glycerol-induced second messenger-operated calcium influx into monocytes from spontaneously hypertensive rats (SHRs) and from normotensive Wistar-Kyoto rats (WKYs). The RNA interference for the downregulation of TRPC3 in monocytes by small, interfering RNA (siRNA) was performed and evaluated using in-cell Western assay.
Thapsigargin-induced, store-operated calcium influx was significantly elevated in SHRs and was approximately double that observed in WKYs. In the presence of nimodipine, the thapsigargin-induced, store-operated calcium influx was also significantly higher in SHRs compared with WKYs. After stimulation of monocytes by angiotensin II, calcium influx was significantly elevated in SHRs, and was approximately double that observed in WKYs. The 1-oleoyl-2-acetyl-sn-glycerol-induced, second messenger-operated calcium influx was also significantly elevated in SHRs compared with WKYs. Thapsigargin-induced, store-operated calcium influx was reduced by the inhibitor 2-aminoethoxydiphenyl borane. After TRPC3 knockdown, the thapsigargin-induced, store-operated calcium influx, as well as 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, was significantly more reduced in cells from SHRs compared with WKYs.
The increased store-operated and second messenger-operated calcium influx through TRPC3 channels in monocytes from SHRs may be responsible for a more aggressive effect in promoting vascular disease in genetic hypertension.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>17903696</pmid><doi>10.1016/j.amjhyper.2007.04.004</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels calcium Calcium - metabolism Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Diglycerides - pharmacology Down-Regulation - drug effects Down-Regulation - physiology Enzyme Inhibitors - pharmacology Experimental diseases hypertension Hypertension - genetics Hypertension - metabolism Male Medical sciences Monocytes Rats Rats, Inbred SHR Rats, Inbred WKY RNA, Small Interfering - pharmacology Second Messenger Systems - drug effects Second Messenger Systems - physiology Thapsigargin - pharmacology Transient receptor potential canonical Type 3 channel TRPC Cation Channels - genetics TRPC Cation Channels - metabolism |
| title | Monocytes From Spontaneously Hypertensive Rats Show Increased Store-Operated and Second Messenger-Operated Calcium Influx Mediated by Transient Receptor Potential Canonical Type 3 Channels |
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