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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\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>, 7 days) in wild-type (WT), Ca<jats:sub>v<\/jats:sub>3.1<jats:sup>\u2212\/\u2212<\/jats:sup>, and Ca<jats:sub>v<\/jats:sub>3.2<jats:sup>\u2212\/\u2212<\/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\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) with and without the mineralocorticoid receptor blocker canrenoate. Ca<jats:sub>v<\/jats:sub>3.1<jats:sup>\u2212\/\u2212<\/jats:sup> and Ca<jats:sub>v<\/jats:sub>3.2<jats:sup>\u2212\/\u2212<\/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>\u2212\/\u2212<\/jats:sup> mice. ANG II increased significantly MAP in WT, Ca<jats:sub>v<\/jats:sub>3.1<jats:sup>\u2212\/\u2212<\/jats:sup>, and Ca<jats:sub>v<\/jats:sub>3.2<jats:sup>\u2212\/\u2212<\/jats:sup> mice with no differences between genotypes. Heart rate was significantly lower in Ca<jats:sub>v<\/jats:sub>3.1<jats:sup>\u2212\/\u2212<\/jats:sup> and Ca<jats:sub>v<\/jats:sub>3.2<jats:sup>\u2212\/\u2212<\/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>\u2212\/\u2212<\/jats:sup> compared with Ca<jats:sub>v<\/jats:sub>3.2<jats:sup>\u2212\/\u2212<\/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>\u2212\/\u2212<\/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>\u2212\/\u2212<\/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>","DOI":"10.1152\/ajprenal.00121.2018","type":"journal-article","created":{"date-parts":[[2019,5,1]],"date-time":"2019-05-01T09:47:24Z","timestamp":1556704044000},"page":"F254-F263","source":"Crossref","is-referenced-by-count":14,"title":["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"],"prefix":"10.1152","volume":"317","author":[{"given":"Anne D.","family":"Thuesen","sequence":"first","affiliation":[{"name":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stine H.","family":"Finsen","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louise L.","family":"Rasmussen","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ditte C.","family":"Andersen","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"},{"name":"Laboratory of Molecular and Cellular Cardiology, Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark"},{"name":"Clinical Institute, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Boye L.","family":"Jensen","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pernille B. 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