Aortic and carotid chemoreceptor responses to metabolic acidosis in the cat.

The effect of metabolic acidosis on the activity of aortic chemoreceptor afferents and their responses to hypoxia and hypercapnia were investigated in nine cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. This effect was compared with that on simultaneously recorded activity of carotid chemoreceptor afferents in three separate cats. The activity of a single or paucifiber preparation of chemoreceptor afferents was recorded at five steady-state levels of arterial O2 tension (PaO2) at a constant arterial CO2 tension (PaCO2) and at three levels of PaCO2 during hyperoxia (PaO2 greater than 400 Torr) before and after slow injection of 1 M lactic acid in the average dose of 2.6 +/- 0.6 mmol X kg-1. On the average, arterial pH decreased from 7.445 +/- 0.046 to 7.222 +/- 0.041 at PaO2 of 98 +/- 5 Torr and PaCO2 of 34 +/- 1 Torr. This decrease in pHa during normoxia increased the aortic chemoreceptor activity from 0.8 +/- 0.2 to 1.4 +/- 0.3 imp X s-1. Metabolic acidosis increased the excitatory effect of hypoxia and hypercapnia. The stimulatory effect of CO2 for the same increase in arterial [H+] was greater than that of metabolic acidosis, indicating a dominant effect of molecular CO2 on aortic chemoreceptors. Simultaneous measurements of carotid and aortic chemoreceptor activities showed that their responses to metabolic acidosis were qualitatively similar. Quantitatively, the response of aortic chemoreceptor afferents was less than that of carotid chemoreceptors.