Aortic body chemoreceptor responses to dopamine, haloperidol, and pargyline

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Abstract
Aortic chemoreceptor activity, from single- or few-fiber afferent nerve preparations, was measured in response to dopamine and a dopaminergic blocker, haloperidol, in 18 anesthetized cats. In 6 of these cats the effect of dopamine was assessed before and after inhibiting monoamine oxidase (MAO) by pargyline. Dopamine infusion (i.v.) (7-14 .mu.g.cntdot.kg-1.cntdot.min-1) had a generally inhibitory effect on aortic chemoreceptor activity, but the magnitude of this effect varied with arterial partial pressure of O2 (PaO2) levels. The inhibitory effect of dopamine increased as PaO2 levels fell, and at severely hypoxic PaO2 levels (< 30 torr), exogenous dopamine had no significant effect. The inhibitory effect of dopamine also increased during hyperoxic hypercapnia. Blockade of dopamine receptors in the aortic body by haloperidol stimulated chemoreceptor activity significantly during hypoxia, suggesting an O2-dependent release of dopamine from the aortic body as PaO2 falls. Inhibition of MAO by pargyline had no significant effect on the control rate of activity at any level of PaO2, but augmented the inhibitory effect of exogenously administered dopamine. MAO is not significantly involved in the degradation of endogenous dopamine at the aortic receptor sites but it may participate in the degradation of exogenous dopamine.