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Am J Physiol Lung Cell Mol Physiol 284: L57-L68, 2003. First published September 6, 2002; doi:10.1152/ajplung.00494.2001
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Vol. 284, Issue 1, L57-L68, January 2003

Inhibitory effects of NO on carotid body: contribution of neural and endothelial nitric oxide synthase isoforms

Viviana Valdés, Matías Mosqueira, Sergio Rey, Rodrigo Del Rio, and Rodrigo Iturriaga

Laboratorio de Neurobiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 1, Chile

We tested the hypothesis that nitric oxide (NO) produced within the carotid body is a tonic inhibitor of chemoreception and determined the contribution of neuronal and endothelial nitric oxide synthase (eNOS) isoforms to the inhibitory NO effect. Accordingly, we studied the effect of NO generated from S-nitroso-N-acetylpenicillamide (SNAP) and compared the effects of the nonselective inhibitor Nomega -nitro-L-arginine methyl ester (L-NAME) and the selective nNOS inhibitor 1-(2-trifluoromethylphenyl)-imidazole (TRIM) on chemosensory dose-response curves induced by nicotine and NaCN and responses to hypoxia (PO2 approx  30 Torr). CBs excised from pentobarbitone-anesthetized cats were perfused in vitro with Tyrode at 38°C and pH 7.40, and chemosensory discharges were recorded from the carotid sinus nerve. SNAP (100 µM) reduced the responses to nicotine and NaCN. L-NAME (1 mM) enhanced the responses to nicotine and NaCN by increasing their duration, but TRIM (100 µM) only enhanced the responses to high doses of NaCN. The amplitude of the response to hypoxia was enhanced by L-NAME but not by TRIM. Our results suggest that both isoforms contribute to the NO action, but eNOS being the main source for NO in the cat CB and exerting a tonic effect upon chemoreceptor activity.

chemoreceptor; nitric oxide


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