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Lowered activation of voltage‐gated sodium channels contributes to blunted baroreflex sensitivity in heart failure rats
Author(s) -
Tu Huiyin,
Zhang Libin,
Tran Thai P.,
Muelleman Robert L.,
Li YuLong
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1051.4
Subject(s) - baroreceptor , baroreflex , medicine , sodium channel , endocrinology , chemistry , neuron , sodium , heart rate , neuroscience , blood pressure , biology , organic chemistry
Voltage‐gated sodium (Na v ) channels are responsible for initiation and propagation of action potential in the neurons. Here we measured the role of Na v channels on aortic baroreceptor neuron excitability and baroreflex sensitivity in sham and CHF rats. CHF was induced by left coronary artery ligation. Immunofluorescent data indicated that Na v 1.7 was expressed in A‐type (myelinated) and C‐type (unmylinated) nodose neurons but Na v 1.8 and Na v 1.9 were expressed only in C‐type nodose neurons. Real‐time RT‐PCR and western blot data showed that CHF reduced mRNA and protein expression levels of Na v channels in nodose neurons. In addition, using the whole cell patch‐clamp technique, we found that Na v current density and cell excitability of the aortic baroreceptor neurons were lower in CHF rats than that in sham rats. Aortic baroreflex sensitivity was blunted in anesthetized CHF rats, compared with that in sham rats. Furthermore, Na v channel activator (rATX II, 100 nM) significantly enhanced Na v current density and cell excitability of aortic baroreceptor neurons and improved aortic baroreflex sensitivity in CHF rats. These results suggest that reduced Na v channel activation is involved in the attenuation of baroreceptor neuron excitability, which subsequently contributes to the impairment of baroreflex in CHF state.