Quantitative Trait Loci Mapping for Intracellular Calcium in Spontaneously Hypertensive Rats
Increased intracellular calcium ([Ca 2+] i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca 2+] i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated...
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| Veröffentlicht in: | American journal of hypertension 2005-05, Vol.18 (5), p.666-671 |
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| creator | Ohno, Yoichi Suzuki, Hiromichi Tanase, Hisao Otsuka, Keiichi Sasaki, Takayuki Suzawa, Taichi Morii, Toshiyuki Ando, Yosuke Maruyama, Tatsuya Saruta, Takao |
| description | Increased intracellular calcium ([Ca
2+]
i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca
2+]
i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated with cardiovascular disease.
In a genome scan, we performed the quantitative trait loci (QTL) mapping for [Ca
2+]
i in back-crossed rats derived from SHR and normotensive Fischer 344 rats, which demonstrated a single major QTL for hypertension on chromosome 1. Thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers was measured in platelets using the Fura-2 method.
Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca
2+]
i were significantly greater in SHR than in Fischer 344 and F
1 rats. The sarco(endo)plasmic reticulum Ca
2+-dependent ATPase II gene locus (
Serca2) between
D12Mgh5 and
D12Mgh6 showed the significant linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and Ca
2+-containing buffers. The peak logarithm of the odds scores were 3.6 and 3.3, respectively. These QTL explained 19.8% and 17.4% of the total variances, respectively.
D3Mit13 and
DXMgh1 showed suggestive linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers, respectively. The peak logarithm of the odds scores were 2.6 and 2.1, respectively.
A significant QTL for [Ca
2+]
i was mapped near
Serca2 on chromosome 12, and suggestive QTL were identified near
D3Mit13 and
DXMgh1 in a genome scan. Genetic abnormalites in platelet [Ca
2+]
i may contribute to cardiovascular disease via platetet hyperactivity, independent of blood pressure elevation. |
| doi_str_mv | 10.1016/j.amjhyper.2004.12.001 |
| format | Article |
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2+]
i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca
2+]
i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated with cardiovascular disease.
In a genome scan, we performed the quantitative trait loci (QTL) mapping for [Ca
2+]
i in back-crossed rats derived from SHR and normotensive Fischer 344 rats, which demonstrated a single major QTL for hypertension on chromosome 1. Thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers was measured in platelets using the Fura-2 method.
Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca
2+]
i were significantly greater in SHR than in Fischer 344 and F
1 rats. The sarco(endo)plasmic reticulum Ca
2+-dependent ATPase II gene locus (
Serca2) between
D12Mgh5 and
D12Mgh6 showed the significant linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and Ca
2+-containing buffers. The peak logarithm of the odds scores were 3.6 and 3.3, respectively. These QTL explained 19.8% and 17.4% of the total variances, respectively.
D3Mit13 and
DXMgh1 showed suggestive linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers, respectively. The peak logarithm of the odds scores were 2.6 and 2.1, respectively.
A significant QTL for [Ca
2+]
i was mapped near
Serca2 on chromosome 12, and suggestive QTL were identified near
D3Mit13 and
DXMgh1 in a genome scan. Genetic abnormalites in platelet [Ca
2+]
i may contribute to cardiovascular disease via platetet hyperactivity, independent of blood pressure elevation.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/j.amjhyper.2004.12.001</identifier><identifier>PMID: 15882549</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 ; Blood Platelets - metabolism ; Blood Pressure ; Calcium - metabolism ; Calcium-Transporting ATPases - genetics ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Experimental diseases ; Female ; Hypertension - genetics ; Hypertension - metabolism ; Intracellular calcium ; Male ; Medical sciences ; Quantitative Trait Loci ; Rats ; Rats, Inbred F344 ; Rats, Inbred SHR ; Rats, Inbred WKY ; Sa gene ; sarco(endo)plasmic reticulum calcium-dependent ATPase II gene ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; spontaneously hypertensive rats</subject><ispartof>American journal of hypertension, 2005-05, Vol.18 (5), p.666-671</ispartof><rights>2005 American Journal of Hypertension, Ltd.</rights><rights>American Journal of Hypertension, Ltd. © 2005 by the American Journal of Hypertension, Ltd. 2005</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group May 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-c0e106cb8e64f28d0e08a1a79a926fb5faf6c32b212ea3d8b6485a1b919435143</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16779079$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15882549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ohno, Yoichi</creatorcontrib><creatorcontrib>Suzuki, Hiromichi</creatorcontrib><creatorcontrib>Tanase, Hisao</creatorcontrib><creatorcontrib>Otsuka, Keiichi</creatorcontrib><creatorcontrib>Sasaki, Takayuki</creatorcontrib><creatorcontrib>Suzawa, Taichi</creatorcontrib><creatorcontrib>Morii, Toshiyuki</creatorcontrib><creatorcontrib>Ando, Yosuke</creatorcontrib><creatorcontrib>Maruyama, Tatsuya</creatorcontrib><creatorcontrib>Saruta, Takao</creatorcontrib><title>Quantitative Trait Loci Mapping for Intracellular Calcium in Spontaneously Hypertensive Rats</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Increased intracellular calcium ([Ca
2+]
i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca
2+]
i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated with cardiovascular disease.
In a genome scan, we performed the quantitative trait loci (QTL) mapping for [Ca
2+]
i in back-crossed rats derived from SHR and normotensive Fischer 344 rats, which demonstrated a single major QTL for hypertension on chromosome 1. Thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers was measured in platelets using the Fura-2 method.
Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca
2+]
i were significantly greater in SHR than in Fischer 344 and F
1 rats. The sarco(endo)plasmic reticulum Ca
2+-dependent ATPase II gene locus (
Serca2) between
D12Mgh5 and
D12Mgh6 showed the significant linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and Ca
2+-containing buffers. The peak logarithm of the odds scores were 3.6 and 3.3, respectively. These QTL explained 19.8% and 17.4% of the total variances, respectively.
D3Mit13 and
DXMgh1 showed suggestive linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers, respectively. The peak logarithm of the odds scores were 2.6 and 2.1, respectively.
A significant QTL for [Ca
2+]
i was mapped near
Serca2 on chromosome 12, and suggestive QTL were identified near
D3Mit13 and
DXMgh1 in a genome scan. Genetic abnormalites in platelet [Ca
2+]
i may contribute to cardiovascular disease via platetet hyperactivity, independent of blood pressure elevation.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Platelets - metabolism</subject><subject>Blood Pressure</subject><subject>Calcium - metabolism</subject><subject>Calcium-Transporting ATPases - genetics</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Intracellular calcium</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Quantitative Trait Loci</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Sa gene</subject><subject>sarco(endo)plasmic reticulum calcium-dependent ATPase II gene</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases</subject><subject>spontaneously hypertensive rats</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqN0dGK1DAUBuAiijuuvsJSEL3rmJM2aXOnzKqzMiLrriiLEE4zqZvaSWuSLs7bm9LRAW_0KjffOefnT5KcAVkCAf6iXeKuvd0P2i0pIcUS6JIQuJcsoCpFBoKw-8mCVIJlJeFwkjzyviURcg4PkxNgVUVZIRbJ18sRbTABg7nT6bVDE9JNr0z6HofB2G9p07v0wgaHSnfd2KFLV9gpM-5SY9OrobcBre5H3-3T9RQnaOunVR8x-MfJgwY7r58c3tPk05vX16t1tvnw9mL1apMpRkXIFNFAuKorzYuGVluiSYWApUBBeVOzBhuuclpToBrzbVXzomIItQBR5AyK_DR5Pu8dXP9j1D7InfFT3jma5GUFkBMe4dO_YNuPzsZsEgjljEMhJsVnpVzvvdONHJzZodtHJKf2ZSt_ty-n9iVQGduPg2eH9WO909vj2KHuCJ4dAHqFXePQKuOPjpelIOXkYHb9OPz_8XSesRhGp_-MYXsbGQMy9ZTNxPigfx6F-x4ryksm119uZEEuz1c3V-_k5-hfzl7Hz7sz8aBXRlult8ZpFeS2N_9K9QurINDj</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>Ohno, Yoichi</creator><creator>Suzuki, Hiromichi</creator><creator>Tanase, Hisao</creator><creator>Otsuka, Keiichi</creator><creator>Sasaki, Takayuki</creator><creator>Suzawa, Taichi</creator><creator>Morii, Toshiyuki</creator><creator>Ando, Yosuke</creator><creator>Maruyama, Tatsuya</creator><creator>Saruta, Takao</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>7X8</scope></search><sort><creationdate>20050501</creationdate><title>Quantitative Trait Loci Mapping for Intracellular Calcium in Spontaneously Hypertensive Rats</title><author>Ohno, Yoichi ; Suzuki, Hiromichi ; Tanase, Hisao ; Otsuka, Keiichi ; Sasaki, Takayuki ; Suzawa, Taichi ; Morii, Toshiyuki ; Ando, Yosuke ; Maruyama, Tatsuya ; Saruta, Takao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-c0e106cb8e64f28d0e08a1a79a926fb5faf6c32b212ea3d8b6485a1b919435143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Platelets - metabolism</topic><topic>Blood Pressure</topic><topic>Calcium - metabolism</topic><topic>Calcium-Transporting ATPases - genetics</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Intracellular calcium</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Quantitative Trait Loci</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Sa gene</topic><topic>sarco(endo)plasmic reticulum calcium-dependent ATPase II gene</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases</topic><topic>spontaneously hypertensive rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ohno, Yoichi</creatorcontrib><creatorcontrib>Suzuki, Hiromichi</creatorcontrib><creatorcontrib>Tanase, Hisao</creatorcontrib><creatorcontrib>Otsuka, Keiichi</creatorcontrib><creatorcontrib>Sasaki, Takayuki</creatorcontrib><creatorcontrib>Suzawa, Taichi</creatorcontrib><creatorcontrib>Morii, Toshiyuki</creatorcontrib><creatorcontrib>Ando, Yosuke</creatorcontrib><creatorcontrib>Maruyama, Tatsuya</creatorcontrib><creatorcontrib>Saruta, Takao</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>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 Edition)</collection><collection>ProQuest Central UK/Ireland</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>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohno, Yoichi</au><au>Suzuki, Hiromichi</au><au>Tanase, Hisao</au><au>Otsuka, Keiichi</au><au>Sasaki, Takayuki</au><au>Suzawa, Taichi</au><au>Morii, Toshiyuki</au><au>Ando, Yosuke</au><au>Maruyama, Tatsuya</au><au>Saruta, Takao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quantitative Trait Loci Mapping for Intracellular Calcium in Spontaneously Hypertensive Rats</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>18</volume><issue>5</issue><spage>666</spage><epage>671</epage><pages>666-671</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>Increased intracellular calcium ([Ca
2+]
i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca
2+]
i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated with cardiovascular disease.
In a genome scan, we performed the quantitative trait loci (QTL) mapping for [Ca
2+]
i in back-crossed rats derived from SHR and normotensive Fischer 344 rats, which demonstrated a single major QTL for hypertension on chromosome 1. Thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers was measured in platelets using the Fura-2 method.
Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca
2+]
i were significantly greater in SHR than in Fischer 344 and F
1 rats. The sarco(endo)plasmic reticulum Ca
2+-dependent ATPase II gene locus (
Serca2) between
D12Mgh5 and
D12Mgh6 showed the significant linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and Ca
2+-containing buffers. The peak logarithm of the odds scores were 3.6 and 3.3, respectively. These QTL explained 19.8% and 17.4% of the total variances, respectively.
D3Mit13 and
DXMgh1 showed suggestive linkage for thrombin-stimulated [Ca
2+]
i in Ca
2+-free and in Ca
2+-containing buffers, respectively. The peak logarithm of the odds scores were 2.6 and 2.1, respectively.
A significant QTL for [Ca
2+]
i was mapped near
Serca2 on chromosome 12, and suggestive QTL were identified near
D3Mit13 and
DXMgh1 in a genome scan. Genetic abnormalites in platelet [Ca
2+]
i may contribute to cardiovascular disease via platetet hyperactivity, independent of blood pressure elevation.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15882549</pmid><doi>10.1016/j.amjhyper.2004.12.001</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0895-7061 |
| ispartof | American journal of hypertension, 2005-05, Vol.18 (5), p.666-671 |
| issn | 0895-7061 1879-1905 1941-7225 |
| language | eng |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Platelets - metabolism Blood Pressure Calcium - metabolism Calcium-Transporting ATPases - genetics Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Experimental diseases Female Hypertension - genetics Hypertension - metabolism Intracellular calcium Male Medical sciences Quantitative Trait Loci Rats Rats, Inbred F344 Rats, Inbred SHR Rats, Inbred WKY Sa gene sarco(endo)plasmic reticulum calcium-dependent ATPase II gene Sarcoplasmic Reticulum Calcium-Transporting ATPases spontaneously hypertensive rats |
| title | Quantitative Trait Loci Mapping for Intracellular Calcium in Spontaneously Hypertensive Rats |
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