Modulatory actions of the gigantocellular reticular nucleus on baroreceptor reflexes in the cat

In chloralose-urethane anesthetized cats, bilateral destruction of the gigantocellular reticular nucleus (GRN) in the medulla oblongata resulted in no discernible alteration of the basal arterial blood pressure and heart rate, as well as no significant influence on the degree of induced reflex bradycardia (by phenylephrine) and reflex tachycardia (by nitroglycerin). Furthermore, prolonged relfex hypertension elicited by a continuous bilateral common carotid artery occlusion was still feasible. Apart from directly promoting cardioinhibition, stimuation of the GRN was capable of interacting synergistically with reflex bradycardia (induced by phenylephrine or angio-transient and antagonistically with reflex tachycardia (induced by nitroglycerin or transient bilateral common carotid artery occlusion). The degree of potentiatioon of reflex bradycardia or suppression of reflex tachycardia by GRN-induced cardio-inhibition was, in most cases, larger than the sum of the individually produced responses. It was also directly related to the dose of the drugs and the intensity of the reticular stimulating train pulses. At the same time, bilateral vagotomy greatly diminished, but did not abolish, these interactions. It is concluded that the GRN may not be a primary component of the neural loop(s) subserving of baroreceptor reflexs. Instead, it may assume a modulatory role on the baroreceptor reflexes, possibly via an action on the autonomic preganglionic neurons.