Acute hypoxia elevates nitric oxide generation in rat carotid body in vitro

In acute hypoxia, the release of nitric oxide (NO) produced in rat carotid body is unclear. The concentration of NO was measured electrochemically wit h a Pt/Nafion/Pd-IrOx/POAP-modified electrode placed on the surface of isol ated carotid bodies superfused with bicarbonate-buffer saline at 35 degrees C. In hypoxia, the concentration of NO in the carotid body was increased by 17 +/-2 nM. The amount of NO release during hypoxia was augmented by incre asing the number of carotid bodies surrounding the electrode and also in th e presence of L-arginine. In addition, the hypoxia-induced elevation of NO was abolished by pretreatment with a nitric oxide synthase (NOS) inhibitor, L-N-G-nitroarginine methylester (L-NAME). The results suggest that endogen ous NO production in the carotid body increases during hypoxia. Electrophys iological measurement of single fiber activity in the sinus nerve revealed that L-NAME treatment enhances the afferent discharge in response to hypoxi a. This confirms that the hypoxia-induced elevation of NO suppresses the ca rotid chemoreceptor response to hypoxia. Taken together, it is concluded th at acute hypoxia increases NO generation in the rat carotid body, and that the elevated levels of NO suppress carotid chemoreceptor activity during hy poxia. Hence, NO may play an active inhibitory role in the control of carot id chemoreceptor activity during hypoxia.