Hif1α-dependent mitochondrial acute O₂ sensing and signaling to myocyte Ca²⁺ channels mediate arterial hypoxic vasodilation.

ABSTRACT: Vasodilation in response to low oxygen (O₂) tension (hypoxic vasodilation) is an essential homeostatic response of systemic arteries that facilitates O₂ supply to tissues according to demand. However, how blood vessels react to O₂ deficiency is not well understood. A common belief is that arterial myocytes are O₂-sensitive. Supporting this concept, it has been shown that the activity of myocyte L-type Ca²⁺channels, the main ion channels responsible for vascular contractility, is reversibly inhibited by hypoxia, although the underlying molecular mechanisms have remained elusive. Here, we show that genetic or pharmacological disruption of mitochondrial electron transport selectively abolishes O₂ modulation of Ca²⁺ c

SUBMITTER: Moreno-Dominguez A 

PROVIDER: S-EPMC11300585 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature