Objective To investigate the changes of cognitive function and hippocampal synaptic plasticity in a mouse model of chronic angiotensin II-dependent hypertension.
Methods We used subcutaneous mini-pumps containing a concentration of angiotensin II (1900 ng/kg/min) that induces malignant hypertension or a saline solution for 28 days. Blood pressure was carefully monitored by a non-invasive tail-cuff method every week throughout the experiment. Long-term potentiation (LTP) was measured by vitro electrophysiology on hippocampal slices at the Schaffer-CA1 pathway, the density and length of the dendritic spines on the CA1 pyramidal cells were examined by confocal microscopy after Golgi staining, and spatial memory was assessed using the Morris water maze test. Data were analysed using SPSS 17.0 software (SPSS, Chicago, USA). All data are presented as mean ± standard deviation and were compared using the paired student's t-test. A P value <0.05 was considered statistically significant.
Results Compared to the saline-treated control group, Ang II significantly raised the systolic blood pressure (p < 0.05) constant throughout the experiment. Hippocampal CA1 LTP was significantly impaired in Ang II-dependent hypertensive mice (102.65 ± 3.14 vs 153.41 ± 5.08, p < 0.01). The density (/30 μm) and length (μm) of the dendritic spines on the CA1 pyramidal cells were reduced in Ang II-dependent hypertensive mice (15.7 ± 2.5 vs 27.3 ± 2.1, p < 0.01; 0.64 ± 0.25 vs 1.01 ± 0.23, p < 0.001). The percentage of time spent in the target quadrant in probe test were significantly reduced in angiotensin II-dependent hypertensive mice (p < 0.05).
Conclusions Hippocampal synaptic plasticity and memory were impaired in angiotensin II-dependent hypertensive mice, supporting the idea that hypertension is a risk factor for cognitive decline.
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