ArticleNeuroreport2019
Inhibitory effects of sulfur dioxide within the nucleus tractus solitarii of rats: involvement of Calcium Ion channels, Adenine nucleoside triphosphate-sensitive potassium channels, and the nitric oxide/cyclic Guanine trinucleotide phosphate pathway.
Article in Neuroreport, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Sulfur Dioxide Alleviates Organ Damage and Inflammatory Response in Cecal Ligation and Puncture-Induced Sepsis Rat.Molecular biotechnology · 2025Article
- Inhibitory effect of sulfur dioxide inhalation on Hering-Breuer inflation reflex in mice: role of voltage-gated potassium channels.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Functional Regulation of KFrontiers in pharmacology · 2022Review
- The role of brain gaseous neurotransmitters in anxiety.Pharmacological reports : PR · 2021Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was designed to investigate the cardiovascular effects of sulfur dioxide within the nucleus tractus solitarii. Sulfur dioxide or artificial cerebrospinal fluid was unilaterally applied into the nucleus tractus solitarii of rats, and the effects on blood pressure, heart rate, and arterial baroreflex sensitivity (ABR) were determined. To explore the mechanisms of the effects of intra-nucleus tractus solitarii sulfur dioxide, various inhibitors were applied prior to sulfur dioxide treatment. Unilateral microinjection of sulfur dioxide produced a dose-dependent decrease in blood pressure in anesthetized rats. Significant decreases in heart rate were also seen after unilateral microinjection of 20 and 200 pmol of sulfur dioxide (P < 0.05). Bilateral microinjection of sulfur dioxide into the nucleus tractus solitarii significantly decreased blood pressure and heart rate and also attenuated ABR. Pretreatment with glibenclamide or nicardipine within the nucleus tractus solitarii did not alter the hypotension or bradycardia (P > 0.05) induced by intra-nucleus tractus solitarii sulfur dioxide. Pretreatment with 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one, however, significantly attenuated this hypotension and bradycardia. Prior application of kynurenic acid or N(G)-Nitro-L-arginine methyl ester into the nucleus tractus solitarii partially diminished the hypotension and bradycardia induced by intra-nucleus tractus solitarii sulfur dioxide. Our present study shows that sulfur dioxide produces cardiovascular inhibitory effects in the nucleus tractus solitarii, predominantly mediated by glutamate receptors and the nitric oxide/cyclic GMP signal transduction pathway.
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