Cardiac denervation does not normalize blunted baroreceptor reflex in heart failure

It is well known that the baroreceptor reflex is significantly blunted in heart failure (HF). It has also been shown that input from cardiac afferents can inhibit the baroreceptor reflex. The aim of the present study was to determine if cardiac afferent input is responsible for the blunted baroreceptor reflex in HF. The rapid pacing HF model (250 beats/min for 4 weeks) was used in this study. Total cardiac denervation was performed on six dogs and 8 dogs served as sham operated control. The acute experiment was carried out after all animals developed severe HF. All dogs were anesthetized with pentobarbital (30 mg/kg, iv). The carotid sinuses were isolated bilaterally and perfused. The aortic nerves and vagi were cut at mid-cervical level. Carotid sinus pressure (CSP)-mean arterial pressure (MAP) and CSP-renal sympathetic nerve activity (RSNA) curves were compared between cardiac denervated and intact dogs with HF. In addition, MAP and RSNA responses to electrical stimulation of the carotid sinus nerve were also compared. Both intact and cardiac denervated HF dogs exhibited a blunted baroreceptor reflex compared to normal intact dogs. The MAP response range to increases in CSP was only 21.8 ± 5.9 mm Hg in intact and 21.5 ± 5.5 mm Hg in cardiac denervated dogs and the RSNA response range to increase in CSP was 68.2 ± 8.8 % of control in intact and 67.7 ± 7.3% of control in cardiac denervated group. There was no difference between intact and cardiac denervated groups in any baroreceptor reflex parameter. Moreover, there was no difference in MAP and RSNA responses to electrical stimulation of the carotid sinus nerve between these two groups. These data suggest that cardiac receptor input is not responsible for the blunted baroreceptor reflex in HF.