title: Nitric oxide as an autocrine regulator of sodium currents in baroreceptor neurons.
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.
authors.affiliation: Department of Physiology and Biophysics, The Cardiovascular Center, The University of Iowa College of Medicine, Iowa City 52242, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Li
authors.forename: M W
authors.initials: MW
authors.lastname: Chapleau
authors.forename: J N
authors.initials: JN
authors.lastname: Bates
authors.forename: K
authors.initials: K
authors.lastname: Bielefeldt
authors.forename: H C
authors.initials: HC
authors.lastname: Lee
authors.forename: F M
authors.initials: FM
authors.lastname: Abboud
mesh_terms: D000818:Animals; D001011:Aorta / Q000294:innervation; D019898:Autocrine Communication / Q000502:physiology*; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000494:pharmacology; D003545:Cysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D004050:Ditiocarb / Q000031:analogs & derivatives / Q000494:pharmacology; D005033:Ethylmaleimide / Q000494:pharmacology; D005296:Ferrous Compounds / Q000494:pharmacology; D006454:Hemoglobins / Q000494:pharmacology; D006834:Hydrazines / Q000494:pharmacology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000737:chemistry / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D009603:Nitroso Compounds / Q000494:pharmacology; D009620:Nodose Ganglion / Q000166:cytology; D018408:Patch-Clamp Techniques; D011311:Pressoreceptors / Q000737:chemistry / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D026403:S-Nitrosothiols; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism; D013439:Sulfhydryl Reagents / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D005296:Ferrous Compounds; D006454:Hemoglobins; D006834:Hydrazines; D009603:Nitroso Compounds; D026403:S-Nitrosothiols; D015222:Sodium Channels; D013439:Sulfhydryl Reagents; C085124:diethyldithiocarbamate iron(II); C016276:8-bromocyclic GMP; D009569:Nitric Oxide; D013779:Tetrodotoxin; C021315:S-nitrosocysteine; D004050:Ditiocarb; D012964:Sodium; D006152:Cyclic GMP; D003545:Cysteine; D005033:Ethylmaleimide