Deficiency of T-type Ca²⁺ channels Cav3.1 and Cav3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice

T-type Ca 2+ channel Ca v 3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Ca v 3.1, but not Ca v 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 −1 ·min −1 , 7 days) in wild-type (WT), Ca v 3.1 −/− , and Ca v 3.2 −/− 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 v 3.2 −/− mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Ca v 3.1 and Ca v 3.2 −/− mice. ANG II increased significantly MAP in WT, Ca v 3.1 −/− , and Ca v 3.2 −/− mice with no differences between genotypes. Heart rate was significantly lower in Ca v 3.1 −/− and Ca v 3.2 −/− mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Ca v 3.1 −/− compared with Ca v 3.2 −/− mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Ca v 3.1 −/− mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Ca v 3.1 −/− 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 v 3.1and Ca v 3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Ca v 3.1, but not Ca v 3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.