Abstract

Epicardial and pericardial sensory nerves mediate cardiac inhibitory (Bezold-Jarisch reflex) as well as cardiac sympathoexcitatory reflexes. Although direct stimulation of cardiac sympathetic afferent nerves influences baroreflex control of blood pressure (BP), the contribution of these cardiac sensory nerves to blood pressure control under normal physiological conditions is not fully clear. In the present study we tested whether elimination of cardiac sympathetic reflexes by intrapericardial (IPC) administration of the neurotoxin resiniferatoxin (RTX) would affect spontaneous blood pressure (BPV) and heart rate variability (HRV) in conscious rats. To this end RTX (15 μg/kg) was administered IPC via a catheter implanted in the pericardial sac of Wistar rats. BP and HR were measured via an indwelling catheter placed in the femoral artery. Cardiac sympathetic deafferentation was verified by comparing the magnitude of pressor responses evoked by IPC applied bradykinin before and after RTX. Using immunohistochemistry the density of CGRP containing nerves in the pericard was compared in vehicle and RTX treated rats (n=3). Cardiac sensory deafferentation by RTX (n=7) did not alter steady state BP and HR as measured in the conscious resting state 3 days before and 3 days after RTX treatment. BPV and HRV were quantified by spectral analysis. The magnitude of the low-frequency and high-frequency components of BPV and HRV were not significantly altered after RTX. These data suggest that cardiac sympathetic afferents do not play a major role in determining BPV and HRV under normal physiological conditions.

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