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This study was designed to define the relative roles of the sympathetic and parasympathetic nervous systems in the reflex alterations of heart rate consequent to changes in arterial pressure. In 23 experiments carried out on 22 anesthetized dogs and in studies performed on four trained, unanesthetized dogs, acute changes in arterial pressure were produced by administering drugs acting on the peripheral vascular bed. The effects of acutely elevating systemic pressure were also investigated in four intact unanesthetized human subjects. Augmenting arterial pressure above control levels with graded doses of phenylephrine always slowed heart rate strikingly. Although complete sympathetic blockade with guanethidine or pronethalol did not significantly alter the degree of slowing, parasympathetic blockade with atropine or vagotomy essentially abolished this response. Conversely, lowering pressure with intravenous injections of nitroglycerin always raised heart rate in the control state, a response abolished by sympathetic blockade with guanethidine or nethalide, but not by parasympathetic blockade with vagotomy or atropine. Thus, when arterial pressure rises above control, the decrease in heart rate is mediated by the parasympathetic nervous system, withdrawal of sympathetic activity playing no detectable role; when pressure falls below control levels, the elevation of heart rate is mediated primarily by the sympathetic nervous system. These findings are not consonant with the traditional concept of control of heart rate which predicates simultaneous reciprocal changes in activity occurring in the two components of the autonomic nervous system.

Relative Roles of the Sympathetic and Parasympathetic Nervous Systems in the Reflex Control of Heart Rate