Rapid resetting of the arterial baroreceptor threshold in the normal circulation extends the pressure range over which baroreflexes operate at high gain. During sustained falls and rises in resting blood pressure (BP), changes in reflex threshold may be greater or less than those of the receptors, through interactions with other sources of afferent drive (e.g. cardiac baroreceptors). In chronic hypertension the magnitude of the reflex resetting again corresponds to that of the arterial baroreceptors, probably because of the resetting of the threshold of the cardiac receptors. 2. 'Baroreflexes' in intact animals are compound reflexes with input from both arterial and non-arterial baroreceptors (e.g. cardiac/pulmonary baroreceptors). The steady-state responses can be characterized by BP-autonomic output function curves, which are often sigmoidal, with a well-defined effector response range and gain. Both sets of input contribute to the high gain component close to resting, with the arterial baroreceptors the major source of reflex drive; the non-arterial baroreceptors also contribute over this part of the reflex and their role increases considerably at high and low BP. 3. In chronic mild/moderate hypertension the changes in baroreflex properties are similar to those of moderate acute rises in BP or in cardiac load; heart rate range of the vagal component of the cardiac baroreflex is depressed, gain is slightly enhanced and the Valsalva-total peripheral resistance (TPR) reflex is unaltered. In severe hypertension: (i) vagal heart rate range and gain are further depressed; and (ii) there is depression of the Valsalva-TPR reflex, much as observed in constrictor reflexes during acute hypertension in normal animals. Circulatory disturbances produce engagement of non-arterial baroreceptors more readily in hypertensives than in normotensives; depression of baroreflexes in hypertension is due partly to enhanced drive from these receptors and partly due to reduction in the gain of the arterial baroreceptors. 4. The reflex vagal depression and that of neural constrictor reflexes can be considered as important homeostatic mechanisms that limit the effects of circulatory perturbations on cardiac filling pressures and on excessive rises in vascular resistance.
