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) 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.NEW & NOTEWORTHY Dexmedetomidine profoundly reshapes baroreflex control beyond its sedative effects. In rats, it markedly reduced the response ranges of arterial pressure, heart rate, and sympathetic nerve activity, while increasing the minimum arterial pressure, a finding consistent with peripheral vasoconstriction. Although these peripheral effects helped preserve operating-point arterial pressure, baroreflex gain was substantially attenuated, suggesting that arterial pressure stability against exogenous disturbances may be compromised during dexmedetomidine sedation.