Acute phosphatidylinositol 4,5 bisphosphate depletion destabilizes sarcolemmal expression of cardiac L-type Ca²⁺ channel Ca_V1.2.

ABSTRACT: Ca_V1.2 channels are critical players in cardiac excitation-contraction coupling, yet we do not understand how they are affected by an important therapeutic target of heart failure drugs and regulator of blood pressure, angiotensin II. Signaling through G_q-coupled AT1 receptors, angiotensin II triggers a decrease in PIP₂, a phosphoinositide component of the plasma membrane (PM) and known regulator of many ion channels. PIP₂ depletion suppresses Ca_V1.2 currents in heterologous expression systems but the mechanism of this regulation and whether a similar phenomenon occurs in cardiomyocytes is unknown. Previous studies have shown that Ca_V1.2 currents are also suppressed by angiotensin II. We hypothesized that these two observati

SUBMITTER: Voelker TL 

PROVIDER: S-EPMC10083594 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature