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Physiological Mechanisms Mediating the Coupling between Heart Period and Arterial
Pressure in Response to Postural Changes in Humans
#MMPMID28396638
Silvani A
; Calandra-Buonaura G
; Johnson BD
; van Helmond N
; Barletta G
; Cecere AG
; Joyner MJ
; Cortelli P
Front Physiol
2017[]; 8
(?): 163
PMID28396638
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The upright posture strengthens the coupling between heart period (HP) and
systolic arterial pressure (SAP) consistently with a greater contribution of the
arterial baroreflex to cardiac control, while paradoxically decreasing cardiac
baroreflex sensitivity (cBRS). To investigate the physiological mechanisms that
mediate the coupling between HP and SAP in response to different postures, we
analyzed the cross-correlation functions between low-frequency HP and SAP
fluctuations and estimated cBRS with the sequence technique in healthy male
subjects during passive head-up tilt test (HUTT, n = 58), during supine
wakefulness, supine slow-wave sleep (SWS), and in the seated and active standing
positions (n = 8), and during progressive loss of 1 L blood (n = 8) to decrease
central venous pressure in the supine position. HUTT, SWS, the seated, and the
standing positions, but not blood loss, entailed significant increases in the
positive correlation between HP and the previous SAP values, which is the
expected result of arterial baroreflex control, compared with baseline recordings
in the supine position during wakefulness. These increases were mirrored by
increases in the low-frequency variability of SAP in each condition but SWS. cBRS
decreased significantly during HUTT, in the seated and standing positions, and
after blood loss compared with baseline during wakefulness. These decreases were
mirrored by decreases in the RMSSD index, which reflects cardiac vagal
modulation. These results support the view that the cBRS decrease associated with
the upright posture is a byproduct of decreased cardiac vagal modulation,
triggered by the arterial baroreflex in response to central hypovolemia.
Conversely, the greater baroreflex contribution to cardiac control associated
with upright posture may be explained, at least in part, by enhanced fluctuations
of SAP, which elicit a more effective entrainment of HP fluctuations by the
arterial baroreflex. These SAP fluctuations may result from enhanced fluctuations
of vascular resistance specific to the upright posture, and not be driven by the
accompanying central hypovolemia.
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