ArticleThe journal of headache and pain2016
Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats.
Article in The journal of headache and pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Heart-Specific Spinal and Vagal Afferents: Transcriptomic Signatures and Optogenetically Modulated Functional Coupling With Cardiomyocytes.Comprehensive Physiology · 2026Article
- Review
- Molecular Anatomy of Synaptic and Extrasynaptic Neurotransmission Between Nociceptive Primary Afferents and Spinal Dorsal Horn Neurons.International journal of molecular sciences · 2025Review
- Chronic Pain Causes Peripheral and Central Responses in MIA-Induced TMJOA Rats.Cellular and molecular neurobiology · 2022Article
- A neuropeptide code for itch.Nature reviews. Neuroscience · 2021Review
- Longitudinal peripheral tissue RNA-Seq transcriptomic profiling, hyperalgesia, and wound healing in the rat plantar surgical incision model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Atrial Natriuretic Peptide Improves Neurite Outgrowth from Spiral Ganglion NeuronsNeural plasticity · 2020Article
- Guanylyl Cyclase A/cGMP Signaling Slows Hidden, Age- and Acoustic Trauma-Induced Hearing Loss.Frontiers in aging neuroscience · 2020Article
- Brain natriuretic peptide (BNP) expressing sensory neurons are not involved in acute, inflammatory or neuropathic pain.Molecular painArticle
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA previous study found that brain natriuretic peptide (BNP) inhibited inflammatory pain via activating its receptor natriuretic peptide receptor A (NPRA) in nociceptive sensory neurons. A recent study found that functional NPRA is expressed in almost all the trigeminal ganglion (TG) neurons at membrane level suggesting a potentially important role for BNP in migraine pathophysiology.
methodsAn inflammatory pain model was produced by subcutaneous injection of BmK I, a sodium channel-specific modulator from venom of Chinese scorpion Buthus martensi Karsch. Quantitative PCR, Western Blot, and immunohistochemistry were used to detect mRNA and protein expression of BNP and NPRA in dorsal root ganglion (DRG) and dorsal horn of spinal cord. Whole-cell patch clamping experiments were conducted to record large-conductance Ca
resultsThe mRNA and protein expression of BNP and NPRA was up-regulated in DRG and dorsal horn of spinal cord after BmK I injection. The BNP and NPRA was preferentially expressed in small-sized DRG neurons among which BNP was expressed in both CGRP-positive and IB4-positive neurons while NPRA was preferentially expressed in CGRP-positive neurons. BNP increased the open probability of BK
conclusionsThese results suggested that BNP might play an important role as an endogenous pain reliever in BmK I-induced inflammatory pain condition. It is also suggested that BNP might play a similar role in other pathophysiological pain conditions including migraine.
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