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Articles in PresS, published online ahead of print September 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00494.2001
Submitted on December 28, 2001
Accepted on August 26, 2002
1 Facultad de Ciencias Biologicas. Laboratorio de Neurobiologia, Pontificia Universidad Catolica de Chile, Santiago, Chile
* To whom correspondence should be addressed. E-mail: riturria{at}bio.puc.cl.
We tested the hypothesis that nitric oxide (NO) produced within the carotid body (CB) is a tonic inhibitor of chemoreception and determined the contribution of neuronal (nNOS) and endothelial (eNOS) nitric oxide synthase 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 N-
-nitro-L-arginine -ethyl-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
30 Torr). CBs excised from pentobarbitone-anaesthetised 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 response to 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.
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