gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Influence of alpha-2 Adrenergic Mechanisms on Baroreflex Buffering

Einfluss alpha-adrenerger Mechanismen auf die Baroreflex Funktion

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker J. Tank
  • A. Diedrich
  • C. Schroeder
  • C. Luft
  • J. Jordan

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP78

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2003/03hoch178.shtml

Veröffentlicht: 11. November 2004

© 2004 Tank et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Systemic norepinephrine transporter inhibition causes a selective dysfunction in the regulation of sympathetic tone, associated with increased sensitivity to vasoactive drugs due to impaired baroreflex buffering. These changes may be mediated by activation of central alpha-2 adrenoreceptors. To test this, we assessed the acute effect of the alpha-2 agonist clonidine on sympathetic vasomotor tone and baroreflex regulation. The subjects were studied once with and once without clonidine. Heart rate, beat-by-beat blood pressure and peroneal nerve activity were determined. Clonidine was applied intravenously (loading dose 150µg, then 20µg/h). Heart rate variability was analyzed in the time and frequency domain. Baroreflex slopes were determined using incremental phenylephrine infusion and nitroprusside. BP was 122±7/73±6 mm Hg at baseline and 100±7/55±3 mm Hg with clonidine (p<0.01). Mean R-R interval increased from 989±77 to 1073±85 ms (p<0.05). Resting MSNA (normalized area under the burst) was 6.0±1.0 a.u. at baseline and 1.8±0.6 a.u. after clonidine. The decrease in MSNA was associated with a reduction in the cold pressor response. Heart rate variability was similar with clonidine compared to baseline. However, increased heart rate variability in the high frequency range during phenylephrine infusion was enhanced with clonidine (1673±548 on control day, vs. 6720±2180 ms² with clonidine). Baroreflex control of heart rate was similar (16 ms/mm Hg) but reset to lower BP and lower heart rate. There was no evidence for impaired baroreflex control of sympathetic vasomotor tone. The dose to reach blood pressure changes of 12.5 mm Hg was unchanged with clonidine (0.58 vs. 0.64 µg/kg/min phenylephrine). We conclude that the alpha-2 mediated sympatholytic effect is not associated with impaired baroreflex blood pressure buffering. Thus, other adrenergic mechanisms are involved in the sympathetic baroreflex dysfunction elicited by norepinephrine transporter inhibition.