NITRIC OXIDE-RELATED INHIBITION OF CAROTID CHEMOSENSORY NERVE ACTIVITY IN THE CAT

The hypothesis that endogenous nitric oxide may play a physiological role in the regulation of carotid chemosensory activity was tested in this study. The nitric oxide synthase (NOS) inhibitors, L-nitro-arginine-methyl ester (L-NAME, 25-200 mu M) and N-G-monomethyl-L-arginine acetate (L-NMMA, 50 and 100 mu M) were used to study its effects on the chemosensory activity of perfused and superfused cat carotid bodies (n = 21)in vitro at 37-37 degrees C. L-NAME elicited slow excitation of the sensory activity as did L-NMMA. The peak-response was dose-dependent, and approached saturation around 200 mu M. The excitation by L-NAME showed the following characteristics (mean +/- SEM): latency of response, 2.2 min +/- 0.3 min; lime to peak response, 5.5 min +/- 1.0 min and the peak response increased to 407 +/- 42 imp/sec from 85 +/- 13 imp/sec. The peak response was significantly different (P < 0.05) from the baseline activity. L-arginine (50-500 mu M) only briefly reversed the stimulation. Hypoxia enhanced the excitation by L-NAME. On the other hand, sodium nitroprusside (SNP, 0.5-10 mu M) which supplies NO, terminated the excitatory effect of L-NAME. The results provide evidence in favor of an inhibitory role of endogenous NO in the carotid body, and exogenous application of NO confirms the inhibitory effect.