Opposing effects of dopamine receptor blockade on ventilation and carotid chemoreceptor activity

To determine the effects of dopamine receptor blockade on the ventilatory responses to hypoxia and hypercapnia we simultaneously measured ventilation and carotid chemoreceptor activity in eight anesthetized cats. During normoxia, haloperidol (1 mg . kg-1 iv) stimulated carotid chemoreceptor activity within 15 s of its administration from a control level of 5.3 +/- 1.1 to 10.4 +/- 2.0 impulses . s-1. Minute ventilation (VI) also rose from 1.00 +/- 0.20 to 1.66 +/- 0.34 l . min-1. Chemoreceptor activity remained elevated, but in the next 15 min VI fell back to or below control levels. Thus haloperidol produced a transient stimulation of ventilation. In the steady state, after haloperidol, carotid chemoreceptor activity was also elevated significantly at all levels of arterial O2 and CO2 partial pressures (PaO2 and PaCO2, respectively). Steady-state ventilation, however, was not significantly different in normoxia (PaO2 82 Torr) after haloperidol despite the elevated chemoreceptor activity. Haloperidol also greatly attenuated the ventilatory response to hypoxia, despite the stimulated carotid chemoreceptor activity. The ventilatory response to hypercapnia was not significantly affected by haloperidol, indicating that its effect was specific for the chemoreflex responses to hypoxia. We conclude that dopamine antagonism by haloperidol blocks the central integration of peripheral chemoreceptor activity, thus attenuating the ventilatory chemoreflex responses to hypoxia while augmenting the carotid chemoreceptor response.