Mechanism of stimulation of aortic chemoreceptors by natural stimuli and chemical substances

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Abstract
Impulses were recorded in single fibres of aortic chemoreceptors of cats anesthetized with chloralose. There was no demonstrable difference between the responses of the endings of medullated and non-medullated fibres respectively to any of the natural stimuli, such as hypoxia, reduction in blood pressure, or reduction in O2 content. This indicates that the generator processes are qualitatively and quantitatively identical at the endings of both types of fibres. Most of the endings were practically silent while ventilating the lungs with air. The maximum frequency of discharge averaged over 4-10 sec while ventilating the lungs with 4% 02 ranged from 1.5 to 24 impulses/sec; in most fibres (21 out of 26 endings) it was less than 12 impulses/sec. All the chemoreceptors tested were considerably stimulated following administration of 0.2 or 2% CO at a time when the 02 content was greater than 4 ml/100 ml. All the chemoreceptors were markedly and rapidly stimulated following circulatory arrest while the cat was ventilated with air. This stimulation fell considerably within 3 min of circulatory arrest. Very little or no excitation followed circulatory arrest while ventilating the cat with pure N2. These results suggest that excitation following circulatory arrest is not produced by a metabolite. There was a remarkable difference between the sensitivities of endings of medullated and non-medullated fibres to drugs. The former were either unaffected by relatively large doses of ACh (100-200 Mg) or phenyl diguanide, or if they were stimulated, the excitation so produced was much less than that produced in endings of non-medullated fibres. This supports the hypothesis that drugs produce their effects by an action at the regenerative regions of the endings, i.e. regions where the nerve impulse is initiated (Paintal, 1964). It also indicates that ACh is not likely to be a transmitter in the normal processes of excitation of chemoreceptors. A mechanism of stimulation of chemoreceptors not involving metabolites is presented.