| First Author | Thuesen AD | Year | 2019 |
| Journal | Am J Physiol Renal Physiol | Volume | 317 |
| Issue | 2 | Pages | F254-F263 |
| PubMed ID | 31042060 | Mgi Jnum | J:280748 |
| Mgi Id | MGI:6369536 | Doi | 10.1152/ajprenal.00121.2018 |
| Citation | Thuesen AD, et al. (2019) Deficiency of T-type Ca(2+) channels Cav3.1 and Cav3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice. Am J Physiol Renal Physiol 317(2):F254-F263 |
| abstractText | T-type Ca(2+) channel Cav3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Cav3.1, but not Cav3.2, 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), Cav3.1(-/-), and Cav3.2(-/-) 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. Cav3.1(-/-) and Cav3.2(-/-) mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Cav3.1 and Cav3.2(-/-) mice. ANG II increased significantly MAP in WT, Cav3.1(-/-), and Cav3.2(-/-) mice with no differences between genotypes. Heart rate was significantly lower in Cav3.1(-/-) and Cav3.2(-/-) mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Cav3.1(-/-) compared with Cav3.2(-/-) mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Cav3.1(-/-) mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Cav3.1(-/-) 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 Cav3.1and Cav3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Cav3.1, but not Cav3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension. |
