Carotid-Cardiac Baroreflex Function Does Not Influence Blood Pressure Regulation during Head-Up Tilt in Humans

Abstract

Abstract:The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40° head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G MAX ), was assessed from the beatto-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 ± 1.0 µg/kg body weight; mean ± SE). In the supine position, glycopyrrolate increased the HR to 91 ± 3 bpm, from 54 ± 3; MAP to 89 ± 2 mmHg, from 76 ± 2; and cardiac output to 6.8 ± 0.3 l·min -1 , from 4.9 ± 0.3 (P < 0.05). The G MAX of the carotid baroreflex control of HR was reduced to -0.06 ± 0.01 bpm·mmHg -1 , from -0.30 ± 0.02 (P < 0.05) with no significant effect on the G MAX of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G MAX of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G MAX of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G MAX of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.Key words: arterial blood pressure, baroreflex, central blood volume, heart rate.The balance between the contribution of the carotid-cardiac and the carotid-vasomotor reflex arms to the carotid baroreflex (CBR) responses to changes in arterial pressure is altered during upright seating compared to the supine position [1]. This change in balance identified that the major adjustment to changes in posture primarily involved the carotid-vasomotor arm of the reflex [1]. This finding confirmed earlier work involving reflex adjustments to reductions in central blood volume (CBV) induced by lower body negative pressure (LBNP) [2]. Furthermore, in average healthy and fit young adults the maximal gains (G MAX ) of the carotid-cardiac and the carotid-vasomotor arms of the CBR were augmented during decreases in CBV [3,4] induced by head-up tilt (HUT) or LBNP [5,6].However, patients who exhibit parasympathetic dysfunction during an orthostatic challenge also exhibit decreased vasomotor responsiveness [7][8][9], indicating that a dysfunction of the carotid-vasomotor arm may be the underlying mechanism of the postural syncope despite the parasympathetic dysfunction. These findings raise the question of whether parasympathetic dysfunctio...

Parallel resetting of arterial baroreflex control of renal and cardiac sympathetic nerve activities during upright tilt in rabbits

“…The parallelism suggests that cardiac sympathetic efferent was a dominant determinant for HR in the present experimental condition with cutting of vagal nerves. Our results could be consistent with the increase in the baroreflex gain for HR assessed by a neck pressure/suction device in humans (11).…”

Gravity, the hydrostatic indifference concept and the cardiovascular system

“…Their activity inhibits cardiovascular centres in the medulla, primarily the nucleus tractus solitarii; this area, in turn, inhibits sympathoexcitatory neurons of the rostral ventrolateral medulla and stimulates parasympathoexcitatory cells in the dorsal vagal nucleus and nucleus ambiguus. The heart rate response to head-up tilt may initially be by vagal withdrawal, arterial pressure is stabilized by increased sympathetic activity (Ogoh et al 2006). The sine of the tilt angle translates into the corresponding hydrostatic pressure gradient, and it determines cardiac baroreflex sensitivity as determined by timedomain signal analysis (Westerhof et al 2006).…”

Baroreflex Function after Spinal Cord Injury

“…28,29 Furthermore, long-term disruption of the cardiovagal baroreflex function has led to increases in blood pressure variability, with little or no influence on mean arterial blood pressure. 30 Resting measures of cardiovagal BRS are also relatively simple to carry out, requiring concurrent recordings of beat-to-beat blood pressure and R-R intervals. As such, the literature is disproportionally represented by studies examining the cardiovagal branch of the baroreflex.…”

“…Although those individuals with complete autonomic failure show severe and marked reductions in blood pressure during orthostatic challenges, blood pressure responses to orthostatic challenges are similar, if not identical, before and after complete vagal efferent blockade. 30,31 Considering Poiseuille's law, blood pressure is affected to the fourth power by arterial diameter, and only linearly by increases in flow (heart rate-derived changes in cardiac output). As such, it is not surprising that the vasomotor branch of the baroreflex is much more important than the vagal branch for the maintenance of mean arterial blood pressure.…”

“…47,48 As such, it is reasonable to suggest that abnormal cardiovagal baroreflex function after SCI is associated with the reduced orthostatic tolerance seen after injury. 30 The loss of the sympathetic branch of the baroreflex is far more detrimental to blood pressure regulation after SCI, as the descending sympathetic pathway becomes disrupted and results in significant reductions in the control of vasomotor tone below the lesion level (Fig. 7).…”