Rad-mediated inhibition of Ca_V1.2 channel activity contributes to uterine artery haemodynamic adaptation to pregnancy.

ABSTRACT: The striking increase of uterine blood flow during pregnancy is essential for normal fetal development as well as for cardiovascular well-being of the mother. Yet, the underlying mechanisms of pregnancy-mediated vasodilatation of the uterine artery are not fully understood. In this study, we test the hypothesis that Rad, a monomeric G protein, is a novel regulatory mechanism in inhibiting Ca_V1.2 channel currents in uterine artery haemodynamic adaptation to pregnancy in a sheep model. We found that pregnancy significantly upregulates Rad expression and decreases Ca_V1.2 channel currents in uterine arterial smooth muscle cells. Rad knockdown ex vivo and in vivo increases Ca_V1.2 activity and channel window currents by reducing steady-state inactivation in uteri

SUBMITTER: Hu XQ 

PROVIDER: S-EPMC11652214 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature