• Respir Physiol Neurobiol · May 2005

    Comparative Study

    Doxapram stimulates the carotid body via a different mechanism than hypoxic chemotransduction.

    • Toru Takahashi, Shinobu Osanai, Hitoshi Nakano, Yoshinobu Ohsaki, and Kenjiro Kikuchi.
    • First Department of Medicine, Asahikawa Medical College, 2-1-1-1 Midorigaoka Higash, Asahikawa 078-8510, Japan. sas@asahikawa-med.ac.jp
    • Respir Physiol Neurobiol. 2005 May 12; 147 (1): 1-9.

    AbstractTo determine if doxapram stimulates the carotid body through the same mechanism as hypoxia, we compared the effects of doxapram and hypoxia on isolated-perfused carotid bodies in rabbits. Doxapram stimulated the carotid body in a dose-dependent manner. In Ca(2+)-free solution, neither doxapram nor hypoxia stimulated the carotid body. Although, doxapram had an additive effect on the carotid body chemosensory response to hypercapnia, a synergistic effect was not observed. Also, we investigated the various K(+) channel activators on the response to doxapram and hypoxia: pinacidil and levcromakalim as ATP-sensitive K(+) channel activators; NS-1619 as a Ca(2+)-sensitive K(+) channel activator; and halothane as a TASK-like background K(+) channel activator. The hypoxic response was partially reduced by halothane only, while pinacidil, levcromakalim and NS-1619 had no effect. Interestingly, the effect of doxapram was partially inhibited by NS-1619. Neither pinacidil nor levcromakalim affected the stimulatory effect of doxapram. We conclude that doxapram stimulates the carotid body via a different mechanism than hypoxic chemotransduction.

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