Carotid chemosensory activity

Chugh DK, Katayama M, Mokashi A, Dehout DE, Ray DK, Lahiri S. Nitric oxide-related inhihition of carotid chemosensory activity in the cat. Respir Physiol 1994 97 147-152. 

Ituniaga R, Larrain C, Zapata P. Effects of dopaminergic blockade upon carotid chemosensory activity and its hypoxia-induced excitation. Brain Res 1994 663 145-154. 

Zapata P. Chemosensory activity in the carotid nerve effects of pharmacological agents. In Gonzalez C, ed. The Carotid Body Chemoreceptors. New "Vork Springer Austin Landes, 1997 119-146. 

Zuazo A, Zapata P. Effects of 6-hydroxy-dopamine on carotid body chemosensory activity. Neurosci Lett 1978 9 323-328. 

When we studied the effects of SNP on carotid chemosensory responses to excitatory and inhibitory stimuh in paralyzed and artificially ventilated cats (15), we found that SNP increased basal chemosensory discharges. This result was completely unexpected, since NO donors reduced or had no effect on basal chemoreceptor activity in the cat CB superfused or perfused in vitro (3-6,16). A major difference between CB preparations in situ and in vitro is the presence of large amounts of endothehum and vascular smooth muscle tissue in situ. Since endothehum and smooth muscle cells are required to activate SNP for releasing NO (27), it is likely that large amounts of NO released from SNP in situ may account for the increased chemosensory activity. 

Heme oxygenase 1 and 2 (HO-1 and HO-2) catalyze the formation of CO and molecular oxygen is required for CO synthesis (67). HO-2 is constitutively expressed in type 1 cells and inhibition of HO-2 by zinc protoporphyrin-9 augments the sensory activity of the carotid body (67). These observations indicate that type I cells of the carotid bodies are capable of producing CO and that CO is inhibitory to the carotid body activity. Consistent with this notion is the findings of Lahiri and Acker (44), who reported that low doses of CO inhibit chemosensory activity of the isolated rat carotid bodies. Future studies may provide insight as to the role of CO in the carotid body function. 

Rimold M, Chemiack NS, Prabhakar NR. Effect of adenosine on chemosensory activity of the cat carotid body. Respir Physiol 1990 80 299-306. 

Natural stimuli of the carotid body (low PO2, acidification) have no effect on PG neurons, but stimuli-related responses can be recorded only in cocultures of carotid body and PG cells. The reconstitution of synaptic contacts between carotid body cells and PG neurons appears to be necessary for the generation of chemosensory activity. 

In a similar vein, Belmonte et al. (17) observed that carotid nerves regenerated into superior cervical ganglia, organs extremely well vascularized, also failed to regain chemoreceptor activity. Therefore, all evidence available suggests that regenerating chemosensory nerve fibers recover chemoreception only when reestablishing contact with carotid body tissue. 

Chemosensory mechanisms in the NTS of rat can develop following irreversible disruption of the chemoafferent pathway. Ventilatory acclimatization to hypoxia was altered but still persisted in carotid sinus nerve-transected rats (106). Since the caudal NTS is a major site of integration for peripheral chemosensory inputs, it is worth noting that the hypoxia-induced increase in tyrosine hydroxylase (TH) mRNA in caudal NTS was not impaired by carotid chemodenervation (106). On the other hand, transsynaptic activation by carotid body inputs is a key element in the changes of norepinephrine turnover during long-term hypoxia since carotid body... 

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