Distinct populations of stretch‐sensitive mechanoreceptors attached to myelinated vagal afferents are found in the heart and adjoining coronary and pulmonary circulations. Receptors at atrio‐venous junctions appear to be involved in control of intravascular volume. These atrial receptors influence sympathetic control of the heart and kidney, but contribute little to reflex control of systemic vascular resistance. Baroreceptors at the origins of the coronary circulation elicit reflex vasodilatation, like feedback control from systemic arterial baroreceptors, as well as having characteristics that could contribute to regulation of mean pressure. In contrast, feedback from baroreceptors in the pulmonary artery and bifurcation is excitatory and elicits a pressor response. Elevation of pulmonary arterial pressure resets the vasomotor limb of the systemic arterial baroreflex, which could be relevant for control of sympathetic vasoconstrictor outflow during exercise and other states associated with elevated pulmonary arterial pressure. Ventricular receptors, situated mainly in the inferior posterior wall of the left ventricle, and attached to unmyelinated vagal afferents, are relatively inactive under basal conditions. However, a change to the biochemical environment of cardiac tissue surrounding these receptors elicits a depressor response. Some ventricular receptors respond, modestly, to mechanical distortion. Probably, ventricular receptors contribute little to tonic feedback control; however, reflex bradycardia and hypotension in response to chemical activation may decrease the work of the heart during myocardial ischaemia. Overall, greater awareness of heterogeneous reflex effects originating from cardiac, coronary and pulmonary artery mechanoreceptors is required for a better understanding of integrated neural control of circulatory function and arterial blood pressure.
Abstract figure legend A schematic illustration of neural inputs to the cardiovascular control centre. The schema provides examples of typical afferent discharge, and related pressure traces, at several locations ( A) and depicts integration of vagal afferent signals arising from systemic arterial baroreceptors, pulmonary arterial baroreceptors, atrial volume receptors, coronary arterial receptors and ventricular receptors ( B). Impulse activity recorded from a pulmonary arterial receptor displays the familiar pattern associated with arterial baroreceptors. Atrial pattern type A displays a volley of impulses that corresponds with atrial systole and a decrease in atrial volume, whereas type B pattern corresponds to atrial diastole and filling of the atrium. Discharge from a coronary mechanoreceptor begins to rise before the aortic pressure and this corresponds the coronary perfusion pulse. Discharge from an unmyelinated vagal afferent increases briskly following injection of veratridine into the aortic root. The table summarizes fibre type, discharge pattern, activating stimuli and reflex effects. *Increase in vagal activity to the heart with no effect on sympathetic activity. #Increase in sympathetic activity to the heart with no effect on vagal activity or inotropy.
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