The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

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The present study aims to systemically characterize the factors that are associated with urinary bladder organ enlargement in spontaneously hypertensive rats (SHR).

Main methods

We compared the SHR to age-matched normotensive Wistar-Kyoto (WKY) control rats in the levels of bladder pro-inflammatory factors, collagen expression (type I), and detrusor smooth muscle growth.

Key findings

Our results showed that enhanced inflammatory responses and fibrosis were key factors that were closely associated with bladder wall thickening in SHR. Specifically the mRNA levels of inflammatory factors interleukin (IL)-1α, IL-6 and TNFα were significantly higher in SHR than those in WKY rats. The SHR also had a higher number of mast cells in the suburothelium space. Type I collagen production was also significantly higher in SHR when compared to that in control rats. However, the smooth muscle content stayed the same in SHR and WKY rats. This was shown by the results that the ratio of α-smooth muscle actin (SMA) to the nuclear protein histone H3 had no difference between these two rat strains. The mRNA and protein levels of proliferating cell nuclear antigen (PCNA) also showed no change in the urinary bladder of SHR and WKY rats. Further study showed that the phosphorylation level of Akt in the urinary bladder was not changed in SHR when compared to WKY rats. In contrast, the phosphorylation level of ERK1/2 was significantly higher in SHR bladder when compared to that of WKY rats.


These results suggest that inflammation and fibrosis are primary factors that may lead to urinary bladder hypertrophy in SHR.

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