Nitric oxide-related inhibition of carotid chemosensory nerve activity in the cat

Abstract

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 μM) and N G - monomethyl- l- arginine acetate ( l-NMMA, 50 and 100 μM) were used to study its effects on the chemosensory activity of perfused and superfused cat carotid bodies ( n = 21) in vitro at 37-37 °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 μM. The excitation by l-NAME showed the following characteristics (mean ± SEM): latency of response, 2.2 min ± 0.3 min time to peak response, 5.5 min ± 1.0 min and the peak response increased to 407 ± 42 mimp/sec from 88 ± 13 imp/sec. The peak response was significantly different ( P<0.05) from the baseline activity. l-arginine (50–500 μM) only brieftly reversed the stimulation. Hypoxia enhanced the excitation by l-NAME. On the other hand, sodium nitroprusside (SNP, 0.5–10 μM) 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.