Adrenergic mechanisms and chemoreception in the carotid body of the cat and rabbit

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Abstract
The effect of .beta.-adrenergic and dopaminergic agonists and antagonists on the chemoreceptor response to graded hypoxia and hypercapnia was tested in 19 cats and 10 rabbits anesthetized either with chloralose-urethane or pentobarbitone sodium, paralyzed with pancuronium bromide and artificially ventilated. The inhibitory action of dopamine was confirmed. The inhibition following intraarterial bolus injection was blocked by haloperidol; dopamine then excited and this excitation was blocked with propranolol. Adrenaline [epinephrine] or noradrenaline [norepinephrine] caused a transient inhibition followed by a marked excitation. The inhibition was blocked with haloperidol and the excitation blocked with propranolol or metoprolol. Isoprenaline excited without inhibition and this was blocked with propranolol or metoprolol. A novel finding was that the chemoreceptor response to hypoxia was markedly reduced or even abolished with propranolol or metoprolol. The response was enhanced with a constant infusion of isoprenaline, adrenaline or noradrenaline in proportion to the degree of hypoxia, an effect mimicked by raising CO2. The chemoreceptor response to hypoxia was similarly enhanced by haloperidol and depressed by a constant infusion of dopamine in proportion to the degree of hypoxia. The effect of these drugs on the chemoreceptor response to hypercapnia was less constant. In the majority of tests the aminergic agonists and antagonists caused a parallel shift of the CO2 response curves in the same direction as the O2 response curves and by amounts proportional to the degree of hypoxia. In some tests these drugs caused a change in the slope of the CO2 response curves, but only if P2O2 [arterial partial pressure] was < 60 mm Hg. Hypoxia may exert a presynaptic action, causing the release of noradrenaline and dopamine from type I cells, and these substances act upon aminergic receptors on the sensory fiber, causing a change in potential and discharge frequency proportional to the rates of dopamine and noradrenaline release; or O2 and CO2 (the latter most probably acting on intracellular pH) may alter the sensitivity of the aminergic receptors to their agonists.