Open AccessNitric oxide and carotid body chemoreception
Author(s) -
Rodrigo Iturriaga
Publication year - 2001
Publication title -
biological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.127
H-Index - 55
eISSN - 0717-6287
pISSN - 0716-9760
DOI - 10.4067/s0716-97602001000200019
Subject(s) - carotid body , chemoreceptor , nitric oxide , inhibitory postsynaptic potential , glomus cell , hypoxia (environmental) , mitochondrion , excitatory postsynaptic potential , biology , respiration , oxidative phosphorylation , nitric oxide synthase , medicine , endocrinology , oxygen , chemistry , neuroscience , microbiology and biotechnology , electrophysiology , anatomy , biochemistry , receptor , organic chemistry
Nitric oxide (NO) has been proposed as an inhibitory modulator of carotid body chemosensory responses to hypoxia. It is believed that NO modulates carotid chemoreception by several mechanisms, which include the control of carotid body vascular tone and oxygen delivery and reduction of the excitability of chemoreceptor cells and petrosal sensory neurons. In addition to the well-known inhibitory effect, we found that NO has a dual (dose-dependent) effect on carotid chemoreception depending on the oxygen pressure level. During hypoxia, NO is primarily an inhibitory modulator of carotid chemoreception, while in normoxia NO increased the chemosensory activity. This excitatory effect produced by NO is likely mediated by an impairment of mitochondrial electron transport and oxidative phosphorylation, which increases the chemosensory activity. The recent findings that mitochondria contain an isoform of NO synthase, which produces significant amounts of NO for regulating their own respiration, suggest that NO may be important for the regulation of mitochondrial energy metabolism and oxygen sensing in the CB.