However, AQP1 was not changed significantly between groups, whereas eNOS expression was significantly decreased after ovariectomy and restored to the control value after estrogen treatment. (p<0.05). The AQP1 and eNOS immunoreactivities were localized in the same areas: capillaries, arterioles, and venules of the lamina propria. The protein expression of AQP1 was not changed significantly, whereas eNOS expression was significantly decreased in the Ovx group and restored to the control value in the Ovx+Est group. == Conclusions == This study showed that ovariectomy causes a significant change in e-NOS expression without a change in AQP1 in menopausal rat urinary bladder. This may imply that e-NOS has a functional role in the bladder overactivity that occurs in association with menopause. Keywords:AQP1, eNOS, Urinary bladder, Menopause == Introduction == The female urinary tracts arise from the urogenital sinus, which is sensitive to sex steroid hormones. Female sex steroid hormone is essential for the ZD-0892 physiological maintenance of the female genitourinary tracts. Postmenopausal women are subject to several urologic dysfunctions, including urinary incontinence, urinary tract infection, and detrusor overactivity [1]. The presence of estrogen receptors throughout the urinary tract and pelvic floor muscle suggests that female sex steroid hormone plays an important role in mediating bladder dysfunction [2]. In an animal study, ovariectomy resulted in bladder mucosal and muscular atrophy, decreased bladder compliance, and decreased detrusor contractility [3]. In clinical ZD-0892 studies, estrogen replacement therapy increased blood flow around the bladder neck in menopausal women and significantly reduced urgency symptoms [4]. Detrusor overactivity is a major cause of urinary tract symptoms and is commonly seen in older menopausal women. A better understanding of the underlying pathophysiology of bladder dysfunction in menopausal women is essential because many patients with menopause suffer from the symptoms itself and related harmful effects on their daily lives and quality of life. The mechanisms for bladder dysfunction in menopausal patients have not yet been fully revealed, and the mechanism involved in the release of neurotransmitters or sensory nerve activation for sensing bladder fullness remains to be evaluated. Aquaporins (AQPs) are a family of water channel proteins that facilitate bidirectional water movement across cell membranes, and in some cases, the movement of glycerol or some solute [5]. Until now, data about Rabbit Polyclonal to ABHD12 AQPs in the mammalian urinary bladder have been limited. Spector et al. [6] investigated the regulation of AQPs in the urothelium of rats following 24 hours of dehydration and water loading tests and reported the localization of AQP1, 2, and 3 in rat urothelium. They suggested that the AQPs in urothelium may play a role in regulating epithelial cell volume and osmolarity. They introduced the possibility of bulk water movement across the urothelium. Also, Rubenwolf et al. [7] demonstrated that AQPs are expressed in cultured human urothelium, suggesting a potential role in transurothelial water and solute transport. However, until now, there have been no studies investigating the expression of AQP family members in the urothelium in an ovariectomy animal model or the functional activity of these proteins in response to hormonal alteration. Combet et al. [8] tried to explain ZD-0892 the role of AQP1 and nitric oxide synthase (NOS) in the peritoneal membrane in experimental ultrafiltration failure in peritoneal dialysis. They suggested that nitric oxide (NO) could modify microvascular permeability by an effective increase in the peritoneal surface area and could regulate plasma membrane proteins such as AQP1 in the peritoneal endothelial cells. NO is thought to play a role in bladder overactivity, which may be associated with impairment in the NO signaling pathway [9]. On the basis of these findings, we hypothesized that AQPs and endothelial NOS (eNOS) might be involved in the physiology of bladder function and dysfunction induced by ovariectomy. The purposes of this study were therefore to investigate the impact of hormonal alteration on AQPs and eNOS isoforms in ZD-0892 rat urinary bladder. == Materials and methods == == Experimental model == Female Sprague-Dawley rats (230~240 g, N=30) were divided into three groups: control (N=10), bilateral ovariectomy (Ovx, N=10), and bilateral ovariectomy followed by subcutaneous injections of 17-estradiol (50 mg/kg/day, Ovx+Est, Sigma Chemical Co., St. Louis, MO, USA, N=10). Animals were premedicated with xylazine (2.2 mg/kg, IM) and anesthetized with a zolazepam/tiletamine cocktail (4.4 mg/kg, IM). The control group underwent a sham operation. The Ovx group underwent a bilateral ovariectomy and was treated with an oil vehicle. The Ovx+Est group underwent a bilateral ovariectomy, followed by treatment with subcutaneous estradiol daily (50 mg/kg/day) for 7 days after ovariectomy. All experimental animals were kept on a standard diet up until the day before.