Investigating feedforward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations in conscious rats.
Investigating feedforward neural regulation
of circulation from analysis of spontaneous arterial pressure and
heart rate fluctuations in conscious rats. Am J Physiol Heart Circ
Physiol 296: H202–H210, 2009. First published November 14, 2008;
doi:10.1152/ajpheart.00358.2008.—It has been suggested in anesthetized
animals that the occurrence of sequences of consecutive beats
characterized by systolic arterial pressure (SAP) and RR or pulse
interval (PI) changing in the opposite direction (SAP /RR and
SAP /RR , nonbaroreflex sequences) might represent the expression
of neural cardiovascular regulatory mechanisms operating with feedforward
characteristics. The aim of the present study was to study
nonbaroreflex sequences in a more physiological experimental model,
i.e., in conscious freely moving rats. We studied conscious rats before
and after 1) complete autonomic blockade (n 12), 2) sympathetic
blockade (n 10), 3) (n 7)- and (n 8)-adrenergic blockade,
and 4) parasympathetic blockade (n 10). Nonbaroreflex sequences
were defined as three or more beats in which SAP and PI of the
following beat changed in the opposite direction. Complete autonomic
blockade reduced the number of nonbaroreflex sequences (95.6 9.0
vs. 45.2 4.1, P 0.001), as did sympathetic blockade (80.9 12.6
vs. 30.9 6.1, P 0.001). The selective -receptor blockade did not
induce significant changes (80.9 12.5 in baseline vs. 79.0 14.7
after prazosin), whereas -receptor blockade significantly reduced
nonbaroreflex sequence occurrence (80.9 12.5 in baseline vs.
48.9 15.3 after propranolol). Parasympathetic blockade produced a
significant increase of nonbaroreflex sequences (95.1 6.9 vs.
136.0 12.4, P 0.01). These results demonstrate the physiological
role of the nonbaroreflex sequences as an expression of a feedforward
type of short-term cardiovascular regulation able to interact dynamically
with the feedback mechanisms of baroreflex origin in the neural
control of the sinus node