Vecuronium Directly Inhibits Hypoxic Neurotransmission of the Rat Carotid Body

UNLABELLED: Previous studies have suggested that partial neuromuscular blockade by vecuronium may inhibit the chemoreceptor neural response to hypoxia. Because acetylcholine and its receptors are critically involved in the hypoxic neurotransmission of the carotid body, we examined whether vecuronium interferes with nicotinic processes in the carotid body and inhibits the chemoreceptor neural response to hypoxia. The carotid body was harvested from anesthetized adult Wister rats. Carotid sinus nerve activity (CSNA) was recorded in vitro, whereas the carotid body was perfused with Krebs solutions equilibrated with 5% CO(2)/air or 5% CO(2)/N(2). Vecuronium (0.1, 0.5, and 5 microM) was administered via perfusion. Hypoxic perfusion increased CSNA and the response remained stable for two hours. With vecuronium 0.5 and 5 microM, the increase in CSNA (DeltaCSNA) in response to hypoxia was significantly attenuated. The inhibitory effect of vecuronium was dose-related. Acetylcholine and nicotine increased CSNA, and the values of DeltaCSNA were significantly attenuated by vecuronium. These results indicate that vecuronium directly inhibits the carotid body neural response to hypoxia, possibly because of the inhibition of neuronal nicotinic receptors in the carotid body. IMPLICATIONS: We investigated the effect of vecuronium on the chemoreceptor response to hypoxia with perfused rat carotid bodies. The results indicate that vecuronium significantly reduces carotid body neural responses to hypoxia, acetylcholine, and nicotine by inhibiting neuronal nicotinic receptors in the carotid body.