Systematic understanding of acute effects of dexmedetomidine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation.

Dexmedetomidine (DEX) is a centrally acting α₂-adrenergic agonist widely used for sedation in emergency and intensive care settings. We examined the effects of DEX on baroreflex-mediated sympathetic regulation of arterial pressure (AP) to distinguish its central and peripheral effects. In anesthetized male Wistar-Kyoto rats (n = 8), baroreflex-mediated changes in sympathetic nerve activity (SNA), AP, and heart rate (HR) were evaluated before and after intravenous DEX administration. DEX (2.5 μg•kg-1) significantly reduced the response ranges of AP (64.4 ± 9.2 to 5.8 ± 3.0 mmHg, P < 0.001), HR (46.5 ± 23.2 to 5.0 ± 6.2 beats/min, P = 0.003), and SNA (87.0 ± 7.5% to 12.6 ± 8.2%, P < 0.001). DEX also decreased the lower limits of HR (325.9 ± 14.6 to 302.2 ± 16.3 beats/min, P < 0.001) and SNA (14.6 ± 6.1% to 1.8 ± 3.0%, P = 0.037) but increased the lower limit of AP (65.4 ± 7.5 to 72.6 mmHg, P = 0.026). Furthermore, DEX reduced both the operating-point AP and gain. Peripheral effects contributed to an increase in operating-point AP (61.7 ± 9.1 vs. 80.9 ± 9.7 mmHg, P = 0.045) but did not affect operating-point gain (0.05 ± 0.08 vs. 0.05 ± 0.08, P = 0.859). In summary, DEX markedly suppressed SNA and induced peripheral vasoconstriction. These peripheral effects contributed to increased minimal AP and preservation of operating-point AP. However, the operating-point gain was substantially reduced, suggesting that AP stability in response to exogenous disturbances may be compromised under DEX sedation.