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Heart rate variability and baroreflex function in AT2 receptor-disrupted mice

Authors

  • V. Gross
  • R. Plehm
  • J. Tank
  • J. Jordan
  • A. Diedrich
  • M. Obst
  • F.C. Luft

Journal

  • Hypertension

Citation

  • Hypertension 40 (2): 207-213

Abstract

  • We adapted telemetry and sequence analysis employed in humans to mice and measured heart rate variability and the spontaneous baroreflex sensitivity in angiotensin II type 2 (AT2) receptor-deleted (AT2 -/-) and wild-type (AT2 +/+) mice with either deoxycorticosterone acetate (DOCA)-salt hypertension or Nw-nitro-L-arginine methylester hydrochloride (L-NAME) hypertension. Mean arterial pressure leveled during the day at 101±1 mm Hg and during the night at 109±1 mm Hg in AT2 receptor-deleted mice, compared with 98±2 mm Hg (day) and 104±2 mm Hg (night) in wild-type mice. Mean arterial pressure increased in AT2 receptor-deleted mice with L-NAME to 114±1 mm Hg (day) and 121±1 mm Hg (night), compared with 105±2 mm Hg (day) and 111±2 mm Hg (night), respectively. DOCA-salt also increased day and night blood pressures in AT2 receptor-deleted mice to a greater degree than in wild-type mice. Heart rate variability in the time and frequency domain was not different between AT2 receptor-deleted mice and AT2 receptor-deleted mice at baseline. Systolic blood pressure variability in the low frequency band was lower in AT2 receptor-deleted mice (0.6±0.1 ms2 versus 3.9±1.3 ms2) than in wild-type mice. Baroreceptor-heart rate reflex sensitivity was significantly increased in AT2 receptor-deleted mice compared with wild-type mice (3.4±0.6 versus 2.1±0.5 ms/mm Hg). These differences remained after DOCA-salt and L-NAME treatments. We conclude that activation of the AT2 receptor impairs arterial baroreceptor reflex function, probably by a central action. These data support the existence of an inhibitory central effect of the AT2 receptor on baroreflex function.


DOI

doi:10.1161/01.HYP.0000027279.69240.75