Abstract

This overview presents four important concepts related to integration of cardiovascular reflexes. 1. 1. Activation of sympathetic efferent activity to various organs is nonuniform. Simultaneous activation of both sympathetic and parasympathetic efferent pathways may occur. These effects are evident in the responses to diving and stimulation of chemoreceptors. Both diving and stimulation of chemoreceptors decrease heart rate and myocardial oxygen demand and cause intense peripheral vasoconstriction, which limits oxygen delivery to the periphery. Stimulation of chemoreceptors also causes active coronary vasodilatation favoring an optimal distribution of blood flow to the heart. 2. 2. When two groups of sensory afferents that cause opposing responses are activated simultaneously, the effect of one sensory afferent system will override the other. During hypotension caused by occlusion of the circumflex coronary artery, the reflexes originating in cardiac vagal afferents are inhibitory and reverse the effect of unloading of arterial baroreceptors. The net effect is not simply blockade of sympathetic vasoconstrictor effects, but withdrawal of sympathetic tone. Thus, the cardiac “reflex” overrides the effects of arterial hypotension. 3. 3. The reflex response to activation of one group of sensory afferents may be dependent on the input from other groups of afferents to the medullary neurons. At low carotid sinus pressure, the “gains” of the chemoreceptor and somatic reflexes are augmented. The cardiopulmonary vagal afferents modulate the arterial baroreceptor reflex as well as the chemoreceptor and somatic reflexes. The cardiopulmonary vagal afferents, when activated, suppress the sympathetic excitatory response to arterial hypotension, to chemoreceptor stimulation and to somatic afferent stimulation. Another important interaction is that of the thermal receptors which, when activated by heat, suppress the vasoconstrictor response to arterial hypotension in cutaneous more than in muscular beds. 4. 4. Stimulation of sensory afferent receptors may be modified by drugs or humoral factors acting on the receptor itself or on the chemical and mechanical characteristics of the tissues surrounding the receptor. Acetylstrophanthidin injected into the circumflex coronary artery potentiates the sympathetic inhibitory response to activation of cardiac sensory afferents (vagal afferents) by volume loading and by occlusion of the circumflex. The sensitization may explain in part the action digitalis has on the peripheral circulation in heart failure. The clinical implications of these four important physiologic concepts are discussed.

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