Abstract
Background: Brain angiotensin II type 1 receptor (AT1R)‐induced pathways (i.e., apoptosis, oxidative stress, and sympathoexcitation) worsen left ventricular (LV) remodeling after myocardial infarction (MI). Although astrocytes were recently suggested to have multiple and important functions in neurovascular unit, normal astrocytes have little AT1R. We hypothesized that MI‐induced abnormal expression of astrocyte AT1R, not neuron, would be a primary cause of worsening LV remodeling.Methods and Results: We generated astrocyte‐specific AT1R knockout mice (astrocyte/AT1R (‐/‐)). In astrocyte/AT1R (+/+) mice at 1 month after MI, we examined brainstem tissues by double immunohistostaining for glial fibrillary acidic protein (GFAP) and AT1R, and determined GFAP positive cells had morphologic changes with increased AT1R expression compared to sham mice without MI. In astrocyte/AT1R (‐/‐) at 1 month after MI, GFAP positive cells with AT1R expression were not observed. LV size at 1 month after MI was smaller in astrocyte/AT1R (‐/‐) than in astrocyte/AT1R (+/+) mice. Heart weight of astrocyte/AT1R (‐/‐) at 1 month after MI was lighter than that of astrocyte/AT1R (+/+) mice.Conclusion: Targeted deletion of AT1R in astrocytes attenuated LV dilatation after MI. These findings suggest that MI‐induced abnormal expression of AT1R in astrocytes is potential primary cause of worsening LV remodeling after MI.
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