Trigeminal‐baroreceptor reflex interactions modulate human cardiac vagal efferent activity.

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Abstract
Instantaneous levels of vagal cardiac inhibition reflect integrated responses of vagal motonuclei to multiple sensory neural inputs. How 2 of these inputs, from trigeminal cutaneous receptors and carotid arterial baroreceptors interact to influence human vagal cardiac outflow, was studied. Nine healthy young men voluntarily maintained breathing rates and tidal volumes within narrow limits. Carotid baroreceptors were stimulated with brief periods of moderate neck suction. Volunteers were studied prone, breathing through a snorkel, before and during face immersion in cold water, and before and after an intravenous injection of a very low dose of atropine sulfate (which increases vagal cardiac efferent activity in dogs). Face immersion raised blood pressure slightly, increased heart period, and augmented baroreflex bradycardia and respiratory sinus arrhythmia significantly. Low-dose atropine together with face immersion further augmented blood pressure, heart period, baroreflex responses and sinus arrhythmia. Evidently, 1 input to the CNS (from trigeminal cutaneous receptors) which increases vagal cardiac outflow, augments vagal responses to another input (from arterial baroreceptors). Since the initial pathways of these 2 inputs are anatomically separate, the influences of respiration and low doses of atropine on vagal motonuclei may be exerted down-stream from the termination of primary trigeminal and baroreceptor afferent fibers.