Alveolar ventilation rises proportionally with metabolic rate during exercise and thus arterial Pco2 remains constant or may even fall slightly. The mechanism underlying this isocapnic hyperpnea, by which ventilation is coupled so precisely to metabolism, however, remains unclear. We have shown recently (Bin-Jaliah et al., 2004), that an increased metabolic rate, induced by insulin infusion, could produce an isocapnic hyperpnoea in an anaesthetized rat and subsequently, we showed that this hyperpnoea was correlated with an increase in the CO2 sensitivity, or gain, of the carotid body such that ventilation could be increased without hypercapnia. Low glucose can stimulate catecholamine release from carotid body tissue (Pardal & Lopez Barneo, 2002) but we demonstrated that the effect we observed in vivo could not be due to an insulin-induced fall in blood glucose concentration (Bin-Jaliah et al., 2005). We speculated that some other blood borne factor may be involved, and we in this present study, we evaluated the role of circulating adrenaline in the augmentation of chemoreceptor gain. Adrenaline has long been mooted as a possible feed forward factor involved in exercise hyperpnoea (Linton et al., 1992) and is know to be released in both hypoglycaemic states (Vollmer et al., 1997) and during exercise (Christensen et al., 1983).
|Title of host publication||The arterial chemoreceptors|
|Editors||Yoshiaki Hayashida , Constancio Gonzalez, Hisatake Kondo|
|Number of pages||6|
|Publication status||Published - 2006|
|Name||Advances in experimental medicine and biology|