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- W2326681417 abstract "INTRODUCTION AND OBJECTIVES: Angiotensin II is reportedly involved in the bladder remodeling underlying bladder dysfunction induced by bladder outlet obstruction, and exerts its effects through angiotensin II type 1 (AT1) and type 2 receptors (AT2). AT1 activation induces organ fibrosis, MAP kinase (MAPK) activation and junctional protein Cx43 expression while AT2 activation increases PPARactivation and adiponectin (Adipo), which protects against AT1-induced fibrosis. This study examined changes in AT1 or AT2 mechanisms in the development of bladder dysfunction during aging. Therefore, we investigated alternations in bladder function and expression of AT1, AT2 and related molecules of the bladder and urethra in aged rats with bladder dysfunction. METHODS: Female SD rats of three different ages at 8 weeks old (8W) (n 5), 9 months old (9M) (n 5) and 15 months old (15M) (n 5) were used. Cystometry was performed under urethane anesthesia, and urodynamic parameters were evaluated, including non-voiding contraction (NVC), pressure threshold (PT), maximum voiding pressure (MVP) and post-void residual volume (RV). After cystometry, the bladder and urethra were excised. The bladder was separated into mucosa and detrusor muscle layers under a microscope. The protein and mRNA expression levels of AT1, Cx43, MAPK, AT2 PPAR, Adipo and adiponectin receptor (Adipo-R) were investigated by Western blot and RT-PCR, respectively. RESULTS: PT, RV and the number of NVCs were significantly increased in 15M vs. 8W rats (P 0.05). MVP was significantly decreased in 15M rats, compared to 8W rats (P 0.05). However, there was no significant difference in any parameters between 8W and 9M rats. In bladder and urethral tissues, the protein and mRNA expression of AT1, Cx43, and MAPK1/2 were significantly increased in 15M than in 8W rats (P 0.05). AT2, PPAR, Adipo, and AdipoR1 were also significantly increased in 15M vs. 8W rats. CONCLUSIONS: These results suggest that, during the aging process, both bladder overactivity and impaired voiding, which are often seen in aged patients, are induced by upregulation of AT1, which can increase Cx43 expression via activation of MAPK signaling pathways. Furthermore, increased adiponectin through PPARactivation, which is regulated by AT2, may protect against AT1-induced bladder fibrosis and dysfunction. Therefore, suppression of AT1 and/or stimulation of PPARvia AT2 could be effective for aged patients with bladder dysfunction." @default.
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- W2326681417 date "2013-04-01" @default.
- W2326681417 modified "2023-09-23" @default.
- W2326681417 title "1944 UPREGULATION OF ANGIOTENSIN II TYPE 1 AND TYPE 2 RECEPTORS IN AGED RATS WITH BLADDER DYSFUNCTION" @default.
- W2326681417 doi "https://doi.org/10.1016/j.juro.2013.02.2363" @default.
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