The Catecholamine Metabolism in Rat Carotid Body: Is there any Efferent Regulation during Long-Term Hypercapnia ?

Abstract

Although hypoxia and hypercapnia are both able to excite the carotid body chemoreceptor activity, several lines of evidence suggest that these two stimuli may operate through different mechanisms (Acker, 1980; Bisgard et al., 1986; Donnelly et al., 1981; Fitzgerald et al., 1983; Mulligan and Lahiri, 1982). In acute hypoxia, dopamine (DA) is released from glomus cells and acts as a neuromodulator of the chemosensory excitation (Hanbauer and Hellström, 1978; Llados and Zapata, 1978). The two catecholamines, DA and norepinephrine (NE), stored in the carotid body are also involved in the chemoreceptor response to long-term hypoxia (Hanbauer et al., 1981; Pequignot et al., 1987). In contrast, there was no release of DA in response to acute hypercapnia (Fitzgerald et al., 1983) and the content of catecholamines in the carotid body remained unchanged after long-term exposure to hypercapnia (Hellström et al., 1989). Because hypercapnia, unlike hypoxia, may be largely sensed by central chemoreceptors, it is conceivable that the carotid chemoreceptor response to hypercapnia may be considerably altered by a potent efferent regulatory influence.