Hif1α-dependent mitochondrial acute O sensing and signaling to myocyte Ca channels mediate arterial hypoxic vasodilation.

Vasodilation in response to low oxygen (O) tension (hypoxic vasodilation) is an essential homeostatic response of systemic arteries that facilitates O supply to tissues according to demand. However, how blood vessels react to O deficiency is not well understood. A common belief is that arterial myocytes are O-sensitive.

Constitutive Expression of Hif2α Confers Acute O Sensitivity to Carotid Body Glomus Cells.

Acute oxygen (O) sensing and adaptation to hypoxia are essential for physiological homeostasis. The prototypical acute O sensing organ is the carotid body, which contains chemosensory glomus cells expressing O-sensitive K channels. Inhibition of these channels during hypoxia leads to cell depolarization, transmitter release, and activation of afferent sensory fibers terminating in the brain stem respiratory and autonomic centers.

Acute O sensing through HIF2α-dependent expression of atypical cytochrome oxidase subunits in arterial chemoreceptors.

Acute cardiorespiratory responses to O deficiency are essential for physiological homeostasis. The prototypical acute O-sensing organ is the carotid body, which contains glomus cells expressing K channels whose inhibition by hypoxia leads to transmitter release and activation of nerve fibers terminating in the brainstem respiratory center. The mechanism by which changes in O tension modulate ion channels has remained elusive.