{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360294646954257536.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1152/ajprenal.00121.2018"}},{"identifier":{"@type":"URI","@value":"https://www.physiology.org/doi/pdf/10.1152/ajprenal.00121.2018"}}],"dc:title":[{"@value":"Deficiency of T-type Ca<sup>2+</sup> channels Ca<sub>v</sub>3.1 and Ca<sub>v</sub>3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p> T-type Ca<jats:sup>2+</jats:sup> channel Ca<jats:sub>v</jats:sub>3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Ca<jats:sub>v</jats:sub>3.1, but not Ca<jats:sub>v</jats:sub>3.2, protects mice against angiotensin II (ANG II)-induced hypertension. Mean arterial blood pressure (MAP) and heart rate were measured continuously with chronically indwelling catheters during infusion of ANG II (30 ng·kg<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>, 7 days) in wild-type (WT), Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup>, and Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice. Plasma aldosterone and renin concentrations were measured by radioimmunoassays. In a separate series, WT mice were infused with ANG II (100 ng·kg<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>) with and without the mineralocorticoid receptor blocker canrenoate. Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup> and Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Ca<jats:sub>v</jats:sub>3.1 and Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice. ANG II increased significantly MAP in WT, Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup>, and Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice with no differences between genotypes. Heart rate was significantly lower in Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup> and Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup> compared with Ca<jats:sub>v</jats:sub>3.2<jats:sup>−/−</jats:sup> mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup> mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Ca<jats:sub>v</jats:sub>3.1<jats:sup>−/−</jats:sup> mice ANG II at 100 ng/kg yielded elevated pressure and an increased heart weight-to-body weight ratio in WT mice. Cardiac hypertrophy, but not hypertension, was prevented by the mineralocorticoid receptor blocker canrenoate. In conclusion, T-type channels Ca<jats:sub>v</jats:sub>3.1and Ca<jats:sub>v</jats:sub>3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Ca<jats:sub>v</jats:sub>3.1, but not Ca<jats:sub>v</jats:sub>3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension. </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380294646954257540","@type":"Researcher","foaf:name":[{"@value":"Anne D. Thuesen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646954257536","@type":"Researcher","foaf:name":[{"@value":"Stine H. Finsen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646954257537","@type":"Researcher","foaf:name":[{"@value":"Louise L. Rasmussen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646954257541","@type":"Researcher","foaf:name":[{"@value":"Ditte C. Andersen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"},{"@value":"Laboratory of Molecular and Cellular Cardiology, Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark"},{"@value":"Clinical Institute, University of Southern Denmark, Odense, Denmark"}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646954257538","@type":"Researcher","foaf:name":[{"@value":"Boye L. Jensen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646954257539","@type":"Researcher","foaf:name":[{"@value":"Pernille B. L. Hansen"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"},{"@value":"Cardiovascular and Metabolic Disease, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Gothenburg, Sweden"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"1931857X"},{"@type":"EISSN","@value":"15221466"}],"prism:publicationName":[{"@value":"American Journal of Physiology-Renal Physiology"}],"dc:publisher":[{"@value":"American Physiological Society"}],"prism:publicationDate":"2019-08-01","prism:volume":"317","prism:number":"2","prism:startingPage":"F254","prism:endingPage":"F263"},"reviewed":"false","url":[{"@id":"https://www.physiology.org/doi/pdf/10.1152/ajprenal.00121.2018"}],"createdAt":"2019-05-01","modifiedAt":"2019-09-21","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050013397240361344","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Calcium channel blocker in patients with chronic kidney disease"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1152/ajprenal.00121.2018"},{"@type":"CROSSREF","@value":"10.1007/s10157-021-02153-1_references_DOI_Ay3MUdTWc8LUHSIR0LKdem21f7S"}]}