Reciprocal modulation of tyrosine hydroxylasea activity in rat carotid body.

The carotid body is an arterial chemoreceptor organ responsive to blood levels of pO2, pCOe and pH 13. The parenchymal tissue of the carotid body is composed mainly of two cell types: the glomus or Type I cells, which are disposed together in groups or glomeruli, and the sustentacular or Type II cells, which appear as glial-like elements enclosing the glomeruli in capsular fashion 3,4. The Type I cells, which have abundant dense-cored vesicles and are known to contain catecholaminesl, 2,11,15, receive a sensory innervation from afferent fibers of the carotid sinus nerve 3. Recent studies have also shown the presence of reciprocal synapses at these junctions between afferent nerve terminals and Type I cells TM. In addition, these cells receive an efferent innervation from both preganglionic and postganglionic sympathetic fibers which reach the carotid body from the superior cervical ganglion 18. The principal catecholamine in the Type I cells of the rat carotid body is dopamine (63 ~), the remainder being norepinephrine 11. Although the precise role of catecholamines in the carotid body remains to be elucidated, there is evidence implicating these substances as neurotransmitters or modulators of chemoreceptor activity 5,6,16,~7,2°,24. Of particular interest are the recent findings in rat carotid body that hypoxia induces a long-term increase in tyrosine hydroxylase (TH) activity, the rate-limiting enzyme in catecholamine biosynthesis 7,9. In these experiments, unanesthetized animals were exposed in a chamber for variable times to low 02 atmospheres. When TH activity was assayed 48 h following the hypoxic episode there was an increase in enzyme activity of 50-80 ~ above control values (control animals were exposed only to room air in the chamber). This long-term induction of TH could have resulted from either direct action by the hypoxic stimulus upon the Type I cells of the carotid body, or instead it might have arisen reflexy via the nervous innervation to the organ. TH activity in other catecholaminergic systems is known to be subject to neural controlS,14,21, 22, and as described above the Type I cells of the carotid body receive a complex nervous innervation (afferent, efferent and reciprocal synapses). It is thus