Oxidative Regulation of Vascular Cav1.2 Channels Triggers Vascular Dysfunction in Hypertension-Related Disorders

Blood pressure is determined by cardiac output and peripheral vascular resistance. The L-type voltage-gated Ca2+ (Ca(v)1.2) channel in small arteries and arterioles plays an essential role in regulating Ca2+ influx, vascular resistance, and blood pressure. Hypertension and preeclampsia are characterized by high blood pressure. In addition, diabetes has a high prevalence of hypertension. The etiology of these disorders remains elusive, involving the complex interplay of environmental and genetic factors. Common to these disorders are oxidative stress and vascular dysfunction. Reactive oxygen species (ROS) derived from NADPH oxidases (NOXs) and mitochondria are primary sources of vascular oxidative stress, whereas dysfunction of the Ca(v)1.2 channel confers increased vascular resistance in hypertension. This review will discuss the importance of ROS derived from NOXs and mitochondria in regulating vascular Ca(v)1.2 and potential roles of ROS-mediated Ca(v)1.2 dysfunction in aberrant vascular function in hypertension, diabetes, and preeclampsia.

Automated summary

This article mainly discusses the importance of ROS derived from NOXs and mitochondria in regulating the Ca(v)1.2 channel in blood vessels, as well as the potential role of ROS-mediated Ca(v)1.2 dysfunction in aberrant vascular function in hypertension, diabetes, and preeclampsia.