AT2 receptor disruption in mice causes slight, non-salt-sensitive hypertension but increases susceptibility to DOCA-salt-induced hypertension.
OBJECTIVES: 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. CONCLUSION: 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.
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Groß et al. (2000) studied Hypertension. Dietary salt loading and DOCA-salt treatment vs. Wild-type mice / baseline was evaluated on Blood pressure, heart rate, aortic pressure dp/dt, locomotor activity, and circadian rhythms.
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