Muscarinic Receptors Influence Catecholamine Release from the Cat Carotid Body During Hypdxia

Abstract

Many frontiers in the modeling of the ventilatory system and its control are at the cellular and molecular levels. The carotid body’s response to hypoxia is no exception to this. A commonly accepted model of the carotid body’s chemotransduction of hypoxia presents the transmitter-laden glomus cell being depolarized by the hypoxic challenge in as-yet-to-be­determined processes. This depolarization activates voltage-gated calcium channels with the subsequent entrance of extracellular calcium. This event, in turn, precipitates the release of several transmitters. Many investigators have reported the hypoxia-generated release of catecholamines from the carotid body. And recently we have reported the release of acetylcholine (ACh) from the cat carotid body during hypoxia¹. These transmitters are presumed to bind to “postsynaptic” receptors located on the apposed sensory afferent fibers which have their cell bodies in the petrosal ganglion with their axons terminating in nucleus tractus solitarii. The transmitters are also presumed to bind to “presynaptic” autoreceptors on the glomus cells. Over the last decade our working hypothesis has been that ACh is the (or at least one) critically important excitatory transmitter. And in the mid 1990s we generated some neurophysiological recordings² which suggested the presence of both M1 and M2 muscarinic receptors in the carotid body. The data could not answer whether the receptors were located postsynaptically, presynaptically, or both. Since then we have reported preliminary results suggesting that they are at least located on the glomus cell.