Contribution of Neural and Endothelial Isoforms of the Nitric Oxide Synthase to the Inhibitory Effects of NO on the Cat Carotid Body

Abstract

Nitric oxide (NO) produced within the carotid body (CB) is an inhibitory modulator of hypoxic chemoreception (Chugh et al., 1994; Wang et al., 1994, 1995; Iturriaga et al, 1998). Administration of NO donors and NO gas to the cat CB reduces the chemosensory response to hypoxia (Chugh et al., 1994; Iturriaga et al., 1998; Iturriaga et al, 2000b). Conversely, the inhibition of nitric oxide synthase (NOS) increases the frequency of carotid chemosensory discharges (f _x) in the cat CB in situ and in vitro (Wang et al., 1994; Iturriaga et al., 1998). It has been proposed that NO produce vasodilatation in the CB (Chugh et al., 1994; Wang et al., 1994; Lahiri and Buerk, 1998), retrograde inhibition of glomus cell’s excitability (Wang et al., 1994), inhibition of glomus cell’s Ca⁺² channels activity (Summers et al., 1999), modulation of petrosal ganglion neurons excitability (Alcayaga et al., 1997), and inhibition of mitochondrial metabolism (Iturriaga et al., 2000b). In the CB, the endothelial NOS (eNOS) is located in the endothelial cells and the neuronal (nNOS) in the sensory terminals of C fibers and parasympathetic neurons (Chugh et al., 1994; Wang et al, 1994, 1995).