ABSTRACT
A major defense mechanism of the mammalian body to acute hypoxia is a rapid increase in inspiratory drive, the so-called acute hypoxic response (AHR). This vital and sometimes life-saving response is aimed at the enhancement of oxygen influx and originates at the peripheral chemoreceptors located in the carotid bodies (CB) [1-3]. In the sense that the CBs are the principal guards of adequate oxygen (and glucose; see Chapter 1 by Nurse, this volume) delivery to the brain, the CBs are strategically located at the bifurcation of the common carotid arteries [1]. The glomus type I cells of the CBs are thought to contain oxygen-sensing mechanisms. The full mechanism of oxygen sensing at the CBs is still poorly understood [2]. At present it is thought that membrane ion channels are critically involved and that low oxygen inhibits Kþ current through the CB type I cell membrane, which causes membrane depolarization and consequently the influx of calcium ions into the cell and the activation of a complex cascade of events within the type I cell ([2] and Chapter 1 by Nurse, this volume). At the end of this cascade, the cell releases neurotransmitters which activate
postsynaptic receptors located on afferent fibers of the sinus nerve that have their cell bodies in the petrosal ganglion (PG) with their axons terminating in the nucleus tractus solitarii (NTS). In the PG, oxygen-sensitive autonomic and sensory neurons give rise to an extensive network of efferent fibers that innervate the CBs [4,5]. These neurons provide nitric oxide-mediated inhibition of the CBs when activated by hypoxia [5] and may play an important role in a negative feedback modulation of the hypoxic ventilatory drive. The peripheral chemoreceptors respond to hypoxia as well as to carbon dioxide and acute metabolic acidosis and, together with the central chemoreceptors located in the ventral medulla, play an important role in maintaining blood gas homeostasis (chemical or metabolic control of breathing) [6].
