TABLE 2:

Summary of the most relevant operational features of the baroreceptor-mediated baroreflexes.

• Changes in transmural pressure stimulate arterial baroreceptors. • Mechanosensitive ion-channels PIEZO1 and PIEZO2, and probably some types of voltage-gated calcium receptors, mediate AP-activation of arterial baroreceptors. • Baroreceptors exert a continuous restraining influence on heart rate and vasoconstrictor tone. • Arterial and cardiopulmonary baroreflexes influence short-term control AP mainly by reducing systemic vascular resistance rather than cardiac output. • Either arterial or cardiopulmonary baroreceptors could be sufficient for normal AP control, and both systems interact for a non-additive attenuation on cardiovascular centers. • Both arterial and cardiopulmonary baroreceptors inhibit sympathetically mediated vasoconstriction, causing vasodilatation; yet, only arterial baroreceptors parasympathetically influence the heart rate. • Chronic activation of arterial baroreceptors can contribute to long-term control of AP by diminishing sympathetic nerve renal activity (and circulating catecholamines), which reduces renin release, sodium reabsorption in the proximal tubule, vasopressin release, and sodium appetite; as a result, urine output increases. • Baroreceptors regulate either the occurrence or the strength of the sympathetic vasoconstrictor tone depending on the vascular bed (e.g., muscle vs. renal) and other moderating factors. • Baroreceptor activation produces a short-latency parasympathetic response on heart rate and a long-latency sympathetic response on vascular smooth muscle tone and myocardial contraction. • Baroreceptor activation exhibits laterality with respect to the side experiencing afferent stimulation. • Baroreceptors stimulation produces a hysteresis effect on vascular and heart rate responses to an increase in AP that is followed by a decrease in AP. • Baroreflex sensitivity (BRS) is the relation (slope) between variations of blood pressure and corresponding changes in cardiovascular effectors (e.g., heart rate, sympathetic vasoconstrictor, myocardial contractions) over time. • The baroreflex effectiveness index (BEI) is the ratio between the number of systolic AP ramps that evoke reflexive heart rate changes and the total number of systolic AP ramps. • Resetting of the baroreflex occurs when there is a change in the reflex operating point to adjust AP to a new level that meets environmental or internal demands (e.g., exercise) or during chronic hypertension. • Electrical field stimulation of the arterial baroreceptors can overcome their resetting and induce reductions in MAP and sympathetic outflow under chronic hypertension. • Baroreflex resetting has more influence on heart rate than on mean AP and systemic vascular resistance. • Changes in BRS generally occur in chronic baroreceptor resetting but usually not during acute resetting. • Baroreceptor resetting can be challenging to detect when vascular distensibility decreases with atherosclerosis or age. • Arterial baroreflexes are active during exercise but undergo resetting by central commands and the exercise pressor reflex. • The exercise pressor reflex begins with the activation of vagal mechanoreceptor (type III) and chemoreceptor (type IV) afferents. • Central commands initiate skeletal muscle contraction at the onset of exercise and inhibit NTS sensitivity to baroreceptor input, which results in a resetting of baroreflexes towards the prevailing pressure evoked by exercise. • The resetting of the arterial baroreflex to resting AP levels at the end of dynamic exercise occurs by the inactivation of central command and activation of cardiopulmonary reflexes. • Cardiopulmonary reflexes counteract exercise pressor reflex by inhibition of the sympathetic vasoconstrictor tone. • Cardiac baroreflexes override vascular baroreflexes to counter exercise evoked hypertensive stimuli. • Close-loop system studies have observed that exercise produces a baroreflex AP-heart rate stimulus-response curve where MAP resets to a higher AP set point with greater maximal response output (i.e., upward and rightward) without changes in the slope of the curves (i.e., constant BRS). • At the onset of exercise, there are dynamic changes in BRS that are effector-dependent in both animals and humans; thus, the gain of the baroreflex is lower for controlling heart rate (atrial sinus node), unchanged for regulating AP (vascular smooth muscle), and higher for modulating sympathetic nerve activity (post-ganglionic sympathetic nerve). • As workload exercise increases in humans, the gain of the baroreflex at the onset decreases for controlling heart rate and increases for modulating muscle sympathetic nerve activity during high intensity isometric or dynamic exercises, whereas it does not change for regulating AP at any intensity level. • The ‘exercise pressor reflex’ and central commands could mediate changes in BRS observed during the time course of exercise. • Open-loop system analysis reveals the differential dynamic properties of two subsystems responding to changes in pressure-load speeds. Baroreceptor input to the NTS activates the neural arc, which results in sympathetic output with fast changes in AP input, producing higher amplitude peripheral sympathetic nerve activity (e.g., high-pass filter). The peripheral arc is the chemical-mechanical coupling between sympathetic nerve endings and the innervated vascular smooth muscle, which determines the systemic AP. The peripheral arc exhibits low-pass filter dynamics such that faster changes in peripheral sympathetic activity have little effect on the systemic AP responses. • During orthostatic stress, the higher transfer function of the neural compensates for the lower transfer function associated with the peripheral arch. • BRS exhibits circadian variations; it is lower in the morning and higher in the evening. • Vagally mediated cardiovascular Bainbridge (tachycardia and hypertension following volume-induced atrial stimulation), and Bezold-Jarisch (bradycardia and hypotension after chemical ventricular stimulation) reflexes blunt arterial baroreflexes. • Cardiopulmonary reflexes suppress both the carotid baroreflexes and chemoreflexes.