Carotid baroreflex control of central and peripheral hemodynamics during recovery after moderate leg cycling exercise

The carotid baroreflex (CBR) control of central and peripheral hemodynamics was investigated after exercise in both the presence and absence of postexercise hypotension (PEH). In individuals with no PEH, the responsiveness of CBR-mediated changes in all hemodynamics was augmented after exercise, particularly to high blood pressure; conversely, the CBR responsiveness remained unchanged in individuals with PEH. These findings provide insight into the mechanism of CBR control after exercise.

Endovascular baroreflex amplification for resistant hypertension: what you need to know

Endovascular baroreflex amplification is an alternative treatment strategy for patients with resistant hypertension. In endovascular baroreflex, the carotid baroreflex is activated by a MobiusHD® device (MD) which has been implanted in the internal carotid artery. This review will discuss the MD technology and mechanism of action and promising results in the first-in-human prospective study involving the use of the MD in patients with resistant hypertension.

Interaction between graviception and carotid baroreflex function in humans during parabolic flight-induced microgravity

The aim of the present study was to assess carotid baroreflex (CBR) function during acute changes in otolithic activity in humans. To address this question, we designed a set of experiments to identify the modulatory effects of microgravity on CBR function at a tilt angle of −2°, which was identified to minimize changes in central blood volume during parabolic flight. During parabolic flight at 0 and 1 g, CBR function curves were modeled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid pulse trains of neck pressure and neck suction ranging from +40 to −80 Torr; CBR control of HR (carotid-HR) and MAP (carotid-MAP) function curves, respectively. The maximal gain of both carotid-HR and carotid-MAP baroreflex function curves were augmented during microgravity compared with 1 g (carotid-HR, −0.53 to −0.80 beats·min−1·mmHg−1, P < 0.05; carotid-MAP, −0.24 to −0.30 mmHg/mmHg, P < 0.05). These findings suggest that parabolic flight-induced acute change of otolithic activity may modify CBR function and identifies that the vestibular system contributes to blood pressure regulation under fluctuations in gravitational forces. NEW & NOTEWORTHY The effect of acute changes in vestibular activity on arterial baroreflex function remains unclear. In the present study, we assessed carotid baroreflex function without changes in central blood volume during parabolic flight, which causes acute changes in otolithic activity. The sensitivity of both carotid heart rate and carotid mean arterial pressure baroreflex function was augmented in microgravity compared with 1 g, suggesting that the vestibular system contributes to blood pressure regulation in humans on Earth.

The carotid baroreflex modifies the pressor threshold of the muscle metaboreflex in humans

The purpose of the present study was to test our hypothesis that unloading the carotid baroreceptors alters the threshold and gain of the muscle metaboreflex in humans. Ten healthy subjects performed a static handgrip exercise at 50% of maximum voluntary contraction. Contraction was sustained for 15, 30, 45, and 60 s and was followed by 3 min of forearm circulatory arrest, during which forearm muscular pH is known to decrease linearly with increasing contraction time. The carotid baroreceptors were unloaded by applying 0.1-Hz sinusoidal neck pressure (oscillating from +15 to +50 mmHg) during ischemia. We estimated the threshold and gain of the muscle metaboreflex by analyzing the relationship between the cardiovascular responses during ischemia and the amount of work done during the exercise. In the condition with unloading of the carotid baroreceptors, the muscle metaboreflex thresholds for mean arterial blood pressure (MAP) and total vascular resistance (TVR) corresponded to significantly lower work levels than the control condition (threshold for MAP: 795 ± 102 vs. 662 ± 208 mmHg and threshold for TVR: 818 ± 213 vs. 572 ± 292 kg·s, P < 0.05), but the gains did not differ between the two conditions (gain for MAP: 4.9 ± 1.7 vs. 4.4 ± 1.6 mmHg·kg·s−1·100 and gain for TVR: 1.3 ± 0.8 vs. 1.3 ± 0.7 mmHg·l−1·min−1·kg·s−1·100). We conclude that the carotid baroreflex modifies the muscle metaboreflex threshold in humans. Our results suggest the carotid baroreflex brakes the muscle metaboreflex, thereby inhibiting muscle metaboreflex-mediated pressor and vasoconstriction responses. NEW & NOTEWORTHY We found that unloading the carotid baroreceptors shifts the pressor threshold of the muscle metaboreflex toward lower metabolic stimulation levels in humans. This finding indicates that, in the normal loading state, the carotid baroreflex inhibits the muscle metaboreflex pressor response by shifting the reflex threshold to higher metabolic stimulation levels.