Long-term blood pressure telemetry in AT2 receptor-disrupted mice.
OBJECTIVE
The hypertension in AT2 receptor knockout mice is imperfectly defined. Therefore, we investigated the influence of dietary salt loading and deoxycorticosterone (DOCA)-salt treatment on blood pressure and diurnal patterns of blood pressure in these mice by radiotelemetry.


METHODS
We used telemetry in AT2 receptor knockout and wild-type mice to measure blood pressure, heart rate, aortic pressure dp/dt, locomotor activity, and circadian rhythms. Salt-related effects were studied by increasing the salt in chow to 4%, adding 1% saline in drinking water, and by DOCA-salt treatment


RESULTS
Baseline blood pressures were higher in AT2 receptor knockout than in wild-type mice and were not affected by increasing the salt intake. The blood pressure increase was steeper and greater in AT2 receptor knockout than in wild-type mice after DOCA-salt treatment A circadian rhythm of blood pressure and heart rate, with higher values during the night, was seen in wild-type, but not in AT2 receptor knockout mice. In AT2 receptor knockout mice, this rhythm was only significant when daily salt intake was increased or when DOCA-salt hypertension was induced. The acrophase of blood pressure and heart rate was found between 2000 and 2400 h and was in accordance with the maximum physical activity.


CONCLUSIONS
These data suggest that AT2 knockout mice display slight hypertension which is not salt-sensitive. On the other hand, the susceptibility to develop DOCA-salt hypertension is increased. The study also illustrates the power of telemetry in monitoring long-term cardiovascular changes and circadian blood pressure and heart rate rhythms in genetically engineered mice.
Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité, Humboldt University of Berlin, Germany.
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Gross
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Milia
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D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D001795:Blood Pressure Determination / Q000379:methods*; D002940:Circadian Rhythm / Q000502:physiology*; D003900:Desoxycorticosterone / Q000633:toxicity; D005500:Follow-Up Studies; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008124:Locomotion / Q000502:physiology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000097:blood*; D012982:Sodium, Dietary / Q000633:toxicity; D013686:Telemetry
D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D012982:Sodium, Dietary; D003900:Desoxycorticosterone