T-type Ca 2+ channel Ca v3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Ca v3.1, but not Ca v3.2, 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 -1·min-1, 7 days) in wild-type (WT), Ca v3.1 -/-, and Ca v3.2 -/- mice. Plasma aldosterone and renin concentrations were measured by radioimmunoassays. In a separate series, WT mice were infused with ANG II (100 ng·kg -1·min-1) with and without the mineralocorticoid receptor blocker canrenoate. Ca v 3.1 -/- and Ca v3.2 -/- mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Ca v3.1 and Ca v3.2 -/- mice. ANG II increased significantly MAP in WT, Ca v3.1 -/-, and Ca v3.2 -/- mice with no differences between geno-types. Heart rate was significantly lower in Ca v3.1 -/- and Ca v3.2 -/- mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Ca v3.1 -/- compared with Ca v3.2 -/- mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Ca v3.1 -/- mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Ca v3.1 -/- 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 v3.1and Ca v3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Ca v3.1, but not Ca v3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.