Effect of chronic volume overload on baroreflex control of heart rate and sympathetic nerve activity.

Baroreceptor-heart rate reflex sensitivity is decreased in congestive heart failure. The reflex control of heart rate and sympathetic nerve activity in rats with chronic volume overload, an established model for moderate heart failure, is still unknown. Therefore, we investigated the regulation of humoral and neuronal sympathetic activity and the baroreflex control of heart rate and sympathetic nerve activity in conscious, unrestrained rats with aortocaval shunt. Rats with aortocaval shunts had larger hearts (388 ± 11 vs. 277 ± 4 mg/100 g body wt), elevated central venous pressures (14 ± 4 vs. 4 ± 3 mmHg), and higher atrial natriuretic peptide plasma levels (87 ± 16 vs. 25 ± 3 pmol/l) than controls but had similar systemic blood pressure and heart rate values. Plasma epinephrine (0.63 ± 0.16 vs. 0.21 ± 0.08 pmol/l, P < 0.05) and norepinephrine concentrations (0.27 ± 0.03 vs. 0.16 ± 0.02 pmol/l, P < 0.05) were elevated in shunted rats compared with controls. Nitroprusside-induced hypotension led to a significantly greater increase in efferent splanchnic sympathetic nerve activity in shunted rats than in controls (0.9 ± 0.1 vs. 2.6 ± 0.6 μV, P < 0.05), whereas the heart rate responses were not different between the groups. These results indicate that the regulation of the autonomic nervous system is altered in chronically volume-overloaded rats. The arterial baroreflex control of efferent splanchnic sympathetic nerve activity was dissociated from the control of heart rate. Therefore, analysis of the activation of sympathetic nervous system assessed by direct measurements of efferent sympathetic nerve activity appears to be more sensitive for the detection of altered autonomic nervous system function than the analysis of baroreflex control of heart rate.