Abstract

In chloralose-urethane anesthetized cats, bilateral destruction of the caudal part of the inferior olivary nucleus (ION) produced neither apparent alteration of the basal arterial blood pressure and heart rate, nor discernible influence on the degree of the induced reflex bradycardia by phenylephrine and reflex tachycardia by nitroglycerin. Apart from directly producing cardioinhibition, stimulation of the ION was capable of interacting synergistically with the reflex bradycardia and antagonistically with the reflex tachycardia. Stimulation of the ION was also capable of potentiating the bradycardias induced from stimulating other cardioinhibitory areas, including the ION of the other side and the gigantocellular reticular nuclei of both sides of the medulla. These interactions were still feasible when one vagus nerve remained intact, but not after both nerves were cut. The results suggest that the ION may not be a primary component of the neural loops subserving the baroreceptor reflex arch, but instead, assumes modulatory actions to this reflex mechanism via both vagus nerves.

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