title: Nitric oxide reduces blood pressure in the nucleus tractus solitarius: a real time electrochemical study.
abstract: Increasing evidence has demonstrated that nitric oxide (NO) is involved in central cardiovascular regulation. In this study, we directly measured extracellular NO levels, in real-time, in the nucleus tractus solitarius (NTS) of anesthetized cats using Nafion/Porphyrine/o-Phenylenediamine-coated NO sensors. We found that local application of L-arginine (L-Arg) induced NO overflow in NTS and hypotension. These responses were potentiated in the vagotomized animals. Pretreatment with NO synthase (NOS)/guanylate cyclase inhibitor methylene blue, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one or NO scavenger hemoglobin attenuated L-Arg-induced hypotension, suggesting that exogenous supplement of NO suppressed cardiac functions through the NOS/cyclic guanosine monophosphate mechanism. The role of endogenous NO was examined after local application of N(G)-nitro-L-arginine methyl ester (L-NAME). We found that L-NAME suppressed endogenous NO levels in NTS and elicited hypertension and tachycardia. Taken together, our data suggest that NO is tonically released in the NTS to inhibit blood pressure.
authors.affiliation: Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
authors.forename: W C
authors.initials: WC
authors.lastname: Wu
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: L S
authors.initials: LS
authors.lastname: Kao
authors.forename: F I
authors.initials: FI
authors.lastname: Tang
authors.forename: C Y
authors.initials: CY
authors.lastname: Chai
mesh_terms: D000818:Animals; D001120:Arginine / Q000494:pharmacology / Q000633:toxicity; D015374:Biosensing Techniques; D001794:Blood Pressure / Q000187:drug effects*; D001919:Bradycardia / Q000139:chemically induced; D002415:Cats; D003199:Computer Systems; D004563:Electrochemistry; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000737:chemistry; D005260:Female; D006157:Guanosine Monophosphate / Q000502:physiology; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors; D006454:Hemoglobins / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced; D007022:Hypotension / Q000139:chemically induced; D008297:Male; D008751:Methylene Blue / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology / Q000633:toxicity; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010069:Oxadiazoles / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects; D011810:Quinoxalines / Q000494:pharmacology; D012018:Reflex / Q000187:drug effects; D012680:Sensitivity and Specificity; D017552:Solitary Nucleus / Q000187:drug effects* / Q000502:physiology; D013610:Tachycardia / Q000139:chemically induced; D014628:Vagotomy
chemical_list: C095284:1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one; D004791:Enzyme Inhibitors; D006454:Hemoglobins; D010069:Oxadiazoles; D011810:Quinoxalines; D009569:Nitric Oxide; D006157:Guanosine Monophosphate; D001120:Arginine; D019001:Nitric Oxide Synthase; D006162:Guanylate Cyclase; D008751:Methylene Blue; D019331:NG-Nitroarginine Methyl Ester