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(Hypertension. 2004;43:1035.)
© 2004 American Heart Association, Inc.

Scientific Contributions

-2 Adrenergic Transmission and Human Baroreflex Regulation

Jens Tank; Andre Diedrich; Elke Szczech; Friedrich C. Luft; Jens Jordan

From the Department of Nephrology and Hypertension (J.T., E.S., F.C.L., J.J.), Franz Volhard Clinic, Medical Faculty of the Charité and HELIOS Klinikum, Berlin, Germany; and the Autonomic Dysfunction Service (A.D.), Vanderbilt University, Nashville, Tenn.

Correspondence to Dr Jens Jordan, Clinical Research Center, Haus 129, Franz-Volhard-Clinic Medical Faculty of the Charité and HELIOS Klinikum, Wiltbergstr. 50, 13125 Berlin, Germany. E-mail jordan{at}fvk.charite-buch.de

We observed earlier that central -2 adrenoceptor stimulation in mice greatly augments parasympathetic tone. To test the effects in humans, we assessed autonomic vasomotor tone and baroreflex regulation in 9 normal young adults on 2 occasions, once with and once without clonidine. We determined heart rate (HR), beat-by-beat blood pressure (BP), and muscle sympathetic nerve activity. HR variability was analyzed in the time and frequency domain. Pharmacological baroreflex slopes were determined using incremental phenylephrine and nitroprusside infusions. Clonidine lowered resting BP (122±4/73±3 versus 100±7/55±3 mm Hg, P<0.01), muscle sympathetic nerve activity (18±3 versus 4±2 bursts/min, P<0.01), and HR (62±3 versus 56±3 bpm, P<0.05). The baroreflex heart rate curve was reset to much lower HR values and showed no saturation at low HR. HR variability profoundly increased during clonidine plus phenylephrine (total power: 3224±843 versus 8943±2329 ms², P<0.05). High-frequency power was 1451±520 at baseline and 6720±2475 ms² during baroreceptor loading (P<0.05). The low-frequency/high-frequency ratio decreased (1.94±0.41 versus 0.69±0.10, P<0.05). In contrast, clonidine reduced resting sympathetic vasomotor tone and shifted the operating point of the sympathetic baroreflex to a flat part of the sympathetic baroreflex curve. The shift decreased the ability of the baroreflex to withdraw sympathetic vasomotor tone during baroreflex loading. These baroreflex changes were associated with a moderate increase in phenylephrine responsiveness. We conclude that -2 adrenoceptor stimulation has a differential effect on baroreflex HR and vasomotor regulation. -2 Adrenoceptor stimulation greatly augments baroreflex-mediated bradycardia, most likely by parasympathetic activation.

Key Words: antihypertensive, agents • blood pressure • heart rate • baroreflex • sympathetic nervous system

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