A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.

ABSTRACT: A Ca²⁺ -activated Cl^- channel protein, ANO1, is expressed in vascular smooth muscle cells where Cl^- current is thought to potentiate contraction by contributing to membrane depolarization. However, there is an inconsistency between previous knockout and knockdown studies on ANO1's role in small arteries. In this study, we assessed cardiovascular function of heterozygous mice with global deletion of exon 7 in the ANO1 gene. We found decreased expression of ANO1 in aorta, saphenous and tail arteries from heterozygous ANO1 knockout mice in comparison with wild type. Accordingly, ANO1 knockdown reduced the Ca²⁺ -activated Cl^- current in smooth muscle cells. Consistent with conventional hypothesis, the contractility of aorta from ANO1 heter

SUBMITTER: Matchkov VV 

PROVIDER: S-EPMC7695021 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature