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Hydrogen Peroxide Mediates Post‐Excitatory Depression of Baroreceptor Afferent Activity in Vivo
Author(s) -
SantanaFilho Valter J,
Abboud Francois M,
Chapleau Mark W
Publication year - 2009
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.23.1_supplement.1008.15
Subject(s) - stimulation , excitatory postsynaptic potential , baroreceptor , chemistry , in vivo , endocrinology , medicine , denervation , catalase , pharmacology , inhibitory postsynaptic potential , blood pressure , oxidative stress , biochemistry , biology , heart rate , microbiology and biotechnology
Acute hypertension leads to 'post‐excitatory depression' (PED) of baroreceptor (BR) activity after the period of elevated blood pressure (BP), a phenomenon that contributes to BR resetting. The molecular mechanism of PED is not fully understood. We recently demonstrated that electrical stimulation of isolated BR neurons in vitro generates reactive oxygen species that cause PED of action potential firing after the period of neuronal activation ( Hypertension 43(6):1349, 2004). In the present study, we tested the hypothesis that the reactive oxygen species hydrogen peroxide (H 2 O 2 ) mediates BR PED in vivo . The left aortic depressor nerve (ADN) was draped over a recording/stimulating electrode and crushed centrally to prevent reflex changes in BP in anesthetized C57BL/6 mice. Afferent ADN (BR) activity was recorded before and after a brief period of ADN stimulation (3V, 2ms pulses at 20Hz for 10s). Afferent BR activity was markedly inhibited after the 10s period of electrical stimulation, averaging 50±5% and 80±8% of baseline levels 5 and 60s after the stimulation was terminated (n=7). This PED was abolished after administration of the membrane permeable H 2 O 2 scavenger PEG‐catalase (4000 U, IV) with activity averaging 100±4 and 126±7% of baseline 5 and 60s after ADN stimulation (n=7). PED was unaffected by administration of the saline vehicle in a separate group of mice (n=6). We conclude that H 2 O 2 generated during activation of BR afferents causes PED. This autocrine‐feedback inhibition of BR activity may contribute to rapid BR resetting in acute hypertension. (HL14388, VA)