H2S, a gasotransmitter for oxygen sensing in carotid body. Focus on “Endogenous H2S is required for hypoxic sensing by carotid body glomus cells”

Abstract

MANY, IF NOT ALL, TISSUES possess the ability to sense hypoxia, and most tissues respond to hypoxia by reducing energy expenditure as a form of self-preservation. The carotid body, however, rapidly responds to hypoxic conditions by initiating cardiorespiratory reflexes in order to increase ventilation and systemic delivery of oxygen rather than initiating mechanisms for local conservation. The carotid body is made up of two types of cells, neuron-like glomus (type 1 cells) and glia-like sustentacular (type II) cells. The glomus cells were identified as the chemoreceptive component of the carotid body nearly 40 years ago in a seminal study by Verna and colleagues (8). Since then, much of the research on the carotid body has been devoted to understanding how glomus cells sense hypoxia and identifying the molecular components of this process. Following the identification of oxygen-sensitive K channels in glomus cells (3), a model of carotid body responsiveness termed the “membrane hypothesis” was developed. Briefly, hypoxia leads to inhibition of K channels, causing membrane depolarization, opening of voltage-dependent Ca 2 channels (VDCC), increasing cytosolic Ca 2 concentration ([Ca 2 ]cyt), and triggering the release of neurotransmitters (7,