Pressor effect of CO2 in the rat: different thresholds of the central cardiovascular and respiratory responses to CO2.

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.