FUNCTIONAL AND DEVELOPMENTAL STUDIES OF THE PERIPHERAL ARTERIAL CHEMORECEPTORS IN RAT - EFFECTS OF NICOTINE AND POSSIBLE RELATION TO SUDDEN-INFANT-DEATH-SYNDROME

The drive on respiration mediated by the peripheral arterial chemorece ptors was assessed by the hyperoxic test in 3-day-old rat pups. They a ccounted for 22.5 +/- 8.8% during control conditions, but only for 6.9 +/- 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotin e reduced dopamine (DA) content and increased the expression of tyrosi ne hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor functi on. During postnatal development TH and DA2R mRNA Levels in the caroti d bodies decreased. Thus, nicotine from smoking may also interfere wit h the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episodes and attenuate the protective chemoreflex response. These mechanisms may underlie the well-known relation between materna l smoking and sudden infant death syndrome.