Impact of dopamine on baroreflex-mediated sympathetic arterial pressure regulation in rats: an open-loop analysis.

Dopamine is commonly used to treat hemodynamic collapse, but its effect on baroreflex-mediated sympathetic arterial pressure (AP) regulation remains to be elucidated. We quantified the effects of dopamine on AP regulation using a baroreflex open-loop analysis by measuring sympathetic nerve activity (SNA) and AP in response to stepwise changes in carotid sinus pressure (CSP) before and during intravenous infusion of dopamine at 2, 10, and 20 µg·kg·min in anesthetized rats ( = 8). We analyzed the CSP-SNA relationship (neural arc) and the SNA-AP relationship (peripheral arc) and constructed a baroreflex equilibrium diagram. The gain at the operating point was calculated from the product of the tangential slope of the neural arc and the slope of the peripheral arc. Compared with baseline, dopamine at 20 µg·kg·min significantly reduced the maximum gain of the neural arc [from 1.898 ± 0.150 to 1.277 ± 0.205%/mmHg ( = 0.014)]. Compared with baseline, dopamine at 10 and 20 µg·kg·min significantly reduced the slope of the peripheral arc [from 0.806 ± 0.079 to 0.645 ± 0.091 mmHg/% ( = 0.031) and 0.633 ± 0.100 mmHg/% ( = 0.020), respectively] and the operating point gain [from 0.800 ± 0.187 to 0.462 ± 0.153 mmHg/mmHg ( = 0.008) and 0.345 ± 0.122 mmHg/mmHg ( < 0.001)] while maintaining the operating point AP. In conclusion, dopamine at 10 and 20 µg·kg·min maintained the operating point AP but significantly reduced the operating point gain for AP regulation, potentially increasing AP variability and instability. Dopamine impaired the arterial pressure (AP) buffering effect mediated by the arterial baroreflex while maintaining AP in anesthetized normal rats. This previously unrecognized effect of dopamine may partially explain why the use of dopamine did not yield favorable outcomes in clinical trials, particularly in patients with shock in whom acute hemodynamic fluctuations can be life-threatening.