Carotid body A decrease in oxygen partial pressure, an increase in carbon dioxide partial pressure, and a decrease in arterial pH can all cause depolarization of the cell membrane, and they affect this by blocking potassium currents. This reduction in the membrane potential opens voltage-gated calcium channels, which causes a rise in intracellular calcium concentration. This causes exocytosis of vesicles containing a variety of neurotransmitters, including acetylcholine, noradrenaline, dopamine, adenosine, ATP, substance P, and met-enkephalin. These act on receptors on the afferent nerve fibres which lie in apposition to the glomus cell to cause an action potential. The feedback from the carotid
Carotid body acid-base transporters (e.g. Na-H) which raise intracellular pH, and activates transporters (e.g. Cl-HCO) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in P sensing. Another mechanism is through oxygen sensitive potassium channels. A drop in dissolved oxygen lead to closing of these channels which results in depolarization. This leads to release of the neurotransmitter dopamine in the glossopharyngeal and vagus afferente to the vasomotor area. The type I (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable.