Deficiency of T-type Ca~(2+) channels Ca_v3.1 and Ca_v3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice

摘要

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-lo-body weight ratio in WT mice. Cardiac hypertrophy, but not hypertension, was prevented by the mineralocorticoid receptor blocker canrenoate. In conclusion, T-lype channels Ca_v3. land Ca_v3.2 do not contribute to baseline blood pressure levels and ANG II-induccd hypertension. Ca_v3.1, but not Ca_v3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.