The carotid bodies, which are the primary sensory organs for sensing changes in arterial blood gases and hydrogen ion concentration, were enlarged in the rat exposed to chronic hypo-, iso-, and hypercapnic hypoxia. In the hypo- and isocapnic hypoxia, the density of VIP fibers increased significantly, and the density of NPY fibers were unchanged. In the hypercapnic hypoxia, the density of NPY fibers was significantly increased, and that of VIP was unchanged. Because these neuropeptides are vasoactive in nature, altered carotid body circulation may contribute to modulation of the chemosensory mechanisms by chronic hypoxia. Three-dimensional analysis showed that these peptidergic fibers are mainly associated with expanded vasculatures. In addition, calbindin D-28k fibers in the hypoxic carotid bodies was significantly decreased. The carotid body one month after the termination of chronic hypoxia was diminished in size, and the density of NPY fibers was increased.
The hypoxia induced either an increase or a decrease in [Ca^<2+>] i in glomus cells. ACh and NaCN mostly increased in [Ca^<2+>] i in glomus cells, and maintained 50% of the amplitude of this [Ca^<2+>] response under the removal of Ca^<2+>. On the basis of these results, we proposed a model of intracellular and cell-to-fiber chemo-transduction in response to chemical stimuli. Relatively large number of glomus cells represent hyperpolarization, while a small number of cells represent depolarization. Gap junction and reciprocal synapses are depicted as important structures for interaction among glomus cells and afferent terminals. Some afferent nerve fibers produced no discharge, since the glomus cells apposed by their terminals do not depolarize, but rather hyperpolarize. A further study is necessary to elucidate what triggers chemo-transduction mechanism.