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Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO 2 : role of carotid body CO 2 (872.3)
Author(s) -
Smith Curtis,
Henderson Kathleen,
Dempsey Jerome
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.872.3
Subject(s) - chemoreceptor , hypocapnia , hypercapnia , central chemoreceptors , carotid body , hypoxic ventilatory response , normocapnia , peripheral chemoreceptors , medicine , stimulation , chemistry , endocrinology , respiratory system , anesthesia , hypoxia (environmental) , oxygen , receptor , organic chemistry
We have shown previously that inhibition of the isolated carotid body (CB) chemoreceptor (via CB‐specific hyperoxia & hypocapnia) markedly reduced the ventilatory response sensitivity of the central chemoreceptors to increased PaCO2 whereas stimulation (via CB‐specific hypoxia & normocapnia) markedly increased it (Blain et al., J. Physiol. 588: 2455‐2471, 2010). These findings were consistent with ventilatory hyperaddition of the CB and central chemoreceptors. We questioned whether changes in CB CO2 alone would result in similar interaction. To date, we have tested this in 4 unanesthetized and chronically instrumented dogs in which the CBs were isolated & perfused independently of the systemic circulation. CB hypocapnia (PcbCO2 ~ 20 mmHg < eupnea; PcbO2 normal) and CB hypercapnia (PcbCO2 ~ 20‐30 mmHg > eupnea; PcbO2 normal) were used to inhibit/stimulate the CB while systemic (and therefore central chemoreceptor) PCO2 was increased with 3 different levels of FICO2 in a normoxic background. We found that CB hypocapnia decreased (mean slope 34% of control), and CB hypercapnia increased (mean slope 125% of control), the ventilatory response of the central chemoreceptors to CO2. Our preliminary conclusion is that the hyperadditive CB/central interaction reported previously is independent of the stimuli used to inhibit/stimulate the CB. Grant Funding Source : Supported by NIH, NHLBI HL50531