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Related Experiment Videos

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

Volkmar Gross1, Ralph Plehm, Jens Tank

  • 1Max-Delbrück-Center for Molecular Medicine, Helios-Klinikum-Berlin, Germany.

Hypertension (Dallas, Tex. : 1979)
|August 3, 2002
PubMed
Summary

Mice lacking the angiotensin II type 2 (AT2) receptor show improved baroreflex function. This suggests the AT2 receptor centrally inhibits the arterial baroreceptor reflex, impacting blood pressure regulation.

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Area of Science:

  • Cardiovascular Physiology
  • Neuroendocrinology
  • Hypertension Research

Background:

  • The angiotensin II type 2 (AT2) receptor's role in cardiovascular regulation, particularly its influence on blood pressure control mechanisms like the baroreflex, remains incompletely understood.
  • Investigating the AT2 receptor's central effects is crucial for understanding its contribution to hypertension and autonomic dysfunction.

Purpose of the Study:

  • To investigate the impact of angiotensin II type 2 (AT2) receptor deletion on heart rate variability and spontaneous baroreflex sensitivity in mice.
  • To determine if AT2 receptor deletion influences blood pressure regulation under hypertensive conditions induced by DOCA-salt or L-NAME.

Main Methods:

  • Adapted telemetry and sequence analysis techniques for use in mice.
  • Measured mean arterial pressure, heart rate variability (time and frequency domains), and spontaneous baroreflex sensitivity in AT2 receptor-deleted (AT2 -/-) and wild-type (AT2 +/+) mice.

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  • Induced hypertension using deoxycorticosterone acetate (DOCA)-salt and N(omega)-nitro-L-arginine methylester hydrochloride (L-NAME).

    • Main Results:

    • AT2 receptor-deleted mice exhibited significantly increased baroreceptor-heart rate reflex sensitivity compared to wild-type mice (3.4±0.6 vs. 2.1±0.5 ms/mm Hg).
    • Systolic blood pressure variability in the low-frequency band was lower in AT2 receptor-deleted mice.
    • These enhanced baroreflex functions in AT2 receptor-deleted mice persisted even after DOCA-salt and L-NAME induced hypertension.

    Conclusions:

    • Activation of the AT2 receptor impairs arterial baroreceptor reflex function, likely through a central mechanism.
    • The AT2 receptor exerts an inhibitory central effect on baroreflex function, contributing to blood pressure regulation.