Nitric oxide as an autocrine regulator of sodium currents in baroreceptor neurons

Zhi Li, Mark W. Chapleau, James N. Bates, Klaus Bielefeldt, Hon Chi Lee, Francois M. Abboud

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Abstract

Arterial baroreceptors are mechanosensitive nerve endings in the aortic arch and carotid sinus that play a critical role in acute regulation of arterial blood pressure. A previous study has shown that nitric oxide (NO) or NO-related species suppress action potential discharge of baroreceptors. In the present study, we investigated the effects of NO on Na+ currents of isolated baroreceptor neurons in culture. Exogenous NO donors inhibited both tetrodotoxin (TTX) -sensitive and -insensitive Na+ currents. The inhibition was not mediated by cGMP but by NO interaction with channel thiols. Acute inhibition of NO synthase increased the Na+ currents. NO scavengers (hemoglobin and ferrous diethyldithiocarbamate) increased Na+ currents before but not after inhibition of NO synthase. Furthermore, NO production in the neuronal cultures was detected by chemiluminescence and immunoreactivity to the neuronal isoform of NO synthase was identified in fluorescently identified baroreceptor neurons. These results indicate that NO/NO-related species function as autocrine regulators of Na+ currents in baroreceptor neurons. Modulation of Na+ channels may represent a novel response to NO.

Original languageEnglish (US)
Pages (from-to)1039-1049
Number of pages11
JournalNeuron
Volume20
Issue number5
DOIs
StatePublished - May 1998

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ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Li, Z., Chapleau, M. W., Bates, J. N., Bielefeldt, K., Lee, H. C., & Abboud, F. M. (1998). Nitric oxide as an autocrine regulator of sodium currents in baroreceptor neurons. Neuron, 20(5), 1039-1049. https://doi.org/10.1016/S0896-6273(00)80484-5