Abstract
The long-acting respiratory stimulant almitrine increases pulmonary ventilation by specifically stimulating the peripheral chemoreceptors. Almitrine was given to 9 dogs via intracarotid injection. Carotid chemoreceptor activity was recorded from single or few-fiber afferent nerve preparations. Doses of 10-20 .mu.g/kg were generally sufficient to produce a brisk stimulatory response of less than 30 min duration. In 4 dogs decreasing arterial PO2 allowed a greater than additive response to almitrine. Infusions of NaHCO3 appeared to depress the response to almitrine whereas changing arterial PCO2 had little effect on the carotid chemoreceptor response to almitrine. Neither dopamine infusion nor dopamine receptor blockade altered the responsiveness of the carotid chemoreceptors to almitrine.