title: Pressor effect of CO2 in the rat: different thresholds of the central cardiovascular and respiratory responses to CO2.
abstract: Rats were anesthetized with urethane and the vagi, aortic and carotid sinus nerves were sectioned bilaterally. Hypocapnia was induced by artificial hyperventilation with 100% O2. Administration of 5% CO2 in O2, without alteration of the respiratory rate or tidal volume, induced significant increases in mean systemic arterial pressure ( mSAP ) in rats with intact central nervous system (CNS) and after midcollicular section (36 +/- 4 and 34 +/- 2 mm Hg, respectively; mean +/- S.E.). Smaller but significant increases in mSAP (17 +/- 3 mm Hg) were induced by inhalation of 5% CO2 after section of the spinal cord at the C4 level. Ganglionic blockade with hexamethonium completely abolished the pressor response to CO2. In hypocapnic (paCO2 15.5 +/- 0.7 mm Hg) apneic rats with intact CNS, after denervation of the peripheral chemoreceptors, inhalation of 1.5% CO2 in O2 increased paCO2 to 22.3 +/- 1.2 mm Hg and mSAP by 16 +/- 1 mm Hg, but the animals remained apneic for up to 45 min of continuous CO2 administration. Higher FICO2s induced further immediate increases in mSAP and, after delays of up to 6-7 min, also a resumption of central rhythmic respiratory activity (monitored by the intercostal muscles or phrenic nerve electrogram). The paCO2 threshold for this respiratory response was 25 +/- 1 mm Hg. When rhythmic respiratory activity resumed, a further slight increase in mSAP and the appearance of respiratory modulated oscillations of the SAP were observed in most animals. When, after a period of CO2 inhalation, 100% O2 was again administered to the animals mSAP fell immediately, reaching the control level within 20-30 s, while the respiratory activity, if present, disappeared only after 1.5-2 min. From these experiments we conclude that in the hypocapnic rat, after denervation of the peripheral chemoreceptors: (1) CO2 induces a neurogenic hypertensive response even in the absence of rhythmic respiratory activity; (2) the central chemosensitive sites appear to be located in the ponto-medullary region and in the spinal cord; and (3) the central mechanisms responsible for the pressor response have a lower CO2 threshold and a much shorter latency than those responsible for the initiation of the rhythmic respiratory activity.
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000494:pharmacology*; D002319:Cardiovascular System / Q000187:drug effects*; D002490:Central Nervous System / Q000187:drug effects*; D002628:Chemoreceptor Cells / Q000187:drug effects; D008526:Medulla Oblongata / Q000187:drug effects; D051381:Rats; D012119:Respiration / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects; D014628:Vagotomy
chemical_list: D002245:Carbon Dioxide