ABSTRACT
PURPOSE: The aim of this study was to evaluate the effect of desmopressin combined with anticholinergics on daytime frequency and urgency in female patients with overactive bladder (OAB). MATERIALS AND METHODS: We included 68 female patients with OAB. Patients were randomly assigned to receive 5 mg of solifenacin (group I) or 5 mg of solifenacin and 0.2 mg of desmopressin (group II) for 2 weeks. A pre/post-treatment 3-day voiding diary and the Urinary Distress Inventory (UDI-6) and Incontinence Impact Questionnaire (IIQ-7) were used to assess changes in voiding symptoms and quality of life (QoL); results were compared between the two groups. RESULTS: Groups I and II included 31 and 37 patients, respectively. Time to first void was 12 min later in group II (105 min vs. 117 min), but this difference was not statistically significant. However, time to the second and third voids (203 min vs. 255 min, 312 min vs. 368 min) and the first urgency episode (212 min vs. 255 min) were significantly longer in group II. Compared with group I, patients in group II showed significant improvement in QoL scores. When improvement after treatment was defined as increase in time to first void of greater than 10% after 2 weeks of treatment, desmopressin with anticholinergics was more effective in patients over the age of 65 years and with more than 150 ml of voided volume. CONCLUSIONS: Desmopressin combined with anticholinergics was more effective than anticholinergics only in the treatment of female patients with OAB.
Subject(s)
Female , Humans , Cholinergic Antagonists , Deamino Arginine Vasopressin , Quality of Life , Quinuclidines , Tetrahydroisoquinolines , Urinary Bladder, Overactive , Solifenacin SuccinateABSTRACT
PURPOSE: The phosphodiesterases (PDEs) are critical components in the cyclic AMP/protein kinase A and the cyclic GMP/phosphokinase G signaling pathways. The cAMP and cGMP pathways are regulated by activation and dissolution of PDEs. Benfotiamine, a lipophilic derivation of thiamine is known an activator of transketolase, is reported to prevent diabetic nephropathy by decreasing proteinuria and reducing oxidative stress. We did this study to investigate the effect of benfotiamine in type 2 diabetic rat kidneys. MATERIALS AND METHODS: We prepared 10 male Long-Evans Tokushima Fatty (LETO: control) and 20 male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which developed non-insulin-dependent diabetes mellitus (NIDDM) naturally. An oral glucose tolerance test confirmed diabetic development in the OLETF rats at 26 weeks. We classified 10 of the OLETF rats into Group I, the no treatment group and the other 10 into Group II, the treatment group. Group II received 100 mg/kg benfotiamine after developing DM. At 44 weeks, we checked kidney weight, serum glucose, free testosterone, insulin, total cholesterol, and triglyceride before sacrifice. We designed the primers for rat PDE5, PDE5A1, and PDE5A2 genes were carried out semiquantitive multiplex RT-PCR. Immunohistochemical staining was performed for monoclonal mouse anti-cGB-PDE5 and mouse monoclonal anti-smooth muscle alpha-actin. RESULTS: For the Control Group, Group I, and Group II, kidney weight was 2.13+/-0.23, 2.08+/-0.22, and 1.94+/-0.44 g; serum glucose was 279.50+/-56.79, 338.00+/-55.00, and 314.71+/-139.1 mg/dl; free testosterone was 1.46+/-1.08, 1.05+/- 0.42, and 0.72+/-0.56 pg/dl; insulin was 1.03+/-0.43, 1.09+/-0.83, and 1.15+/-1.08 ng/ml; total cholesterol was 86.83+/-4.79, 132.00+/-7.69, and 118.14+/-30.93 mg/dl; and triglyceride was 78.83+/-16.47, 177.83+/-75.62, and 194.57+/-92.57 mg/dl, respectively. All three groups expressed PDE5, PDE5A1, PDE5A2 mRNA, but Group I PDE5 mRNA expression was lower than that of Group C, II. However, the expression of PDE5A1 and PDE5A2 mRNA was not significantly different among the three groups. CONCLUSIONS: Serum cholesterol, triglyceride, and glucose were significantly higher in OLETF than in LETO rats. The PDEs were lower in diabetic rat (OLETF) kidneys and PDEs may play a significant role in the development of diabetic renal complications. Benfotiamine is suggested to increase expression of PDE5 mRNA in the type 2 diabetes rat kidney, but the difference in expression levels between PDE5A1 and PDE5A2 was not significant. These findings suggest that benfotiamine may play a specific role in diabetic changes of the rat kidney via a PDE5-related pathway, but it is not clear whether subtype PDE5A1 and PDE5A2 genes play a specific role.
Subject(s)
Animals , Humans , Male , Mice , Rats , Actins , Cholesterol , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Diethylstilbestrol , Glucose , Glucose Tolerance Test , Insulin , Kidney , Muscles , Oxidative Stress , Phosphoric Diester Hydrolases , Phosphotransferases , Protein Isoforms , Proteinuria , Rats, Inbred OLETF , RNA, Messenger , Testosterone , Thiamine , TransketolaseABSTRACT
PURPOSE: To investigate the tissue distribution of PDE5 isoforms in type 2 diabetic rat penile tissues. MATERIALS AND METHODS: We prepared ten male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which develop NIDDM naturally, and ten control male Long-Evans Tokushima Fatty (LETO) rats. An oral glucose tolerance test confirmed diabetes development in OLETF rats at 26 weeks. At 42 weeks, we checked serum glucose, testosterone, triglyceride, insulin, and adiponectin before sacrifice. We performed semi-quantitative multiplex RT-PCR for rat PDE5, PDE5A1, and PDE5A2. Immunohistochemistry was performed using mouse monoclonal anti-cGB-PDE5 and anti-smooth muscle alpha-actin. RESULTS: OLETF rats were significantly more hyperglycemic, hypogonadal, hyperinsulinemic, hypercholesterolemic, hypertriglycemic, and had lower adiponectin levels than LETO rats. Levels of PDE5 mRNA were decreased in OLETF rats, but there were no changes in PDE5A1 or PDE5A2 mRNA levels. CONCLUSION: Diabetes may contribute to decreased expression of PDE5 mRNA, but not PDE5A1 or PDE5A2, in rat penile tissue. Furthermore, serum free testosterone was decreased in diabetic rats. PDE5 has an important role in the development of diabetic erectile dysfunction, but it is not clear whether PDE5A1 and PDE5A2 gene have specific roles.
Subject(s)
Animals , Humans , Male , Mice , Rats , Actins , Adiponectin , Cyclic Nucleotide Phosphodiesterases, Type 5 , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Erectile Dysfunction , Glucose , Glucose Tolerance Test , Immunohistochemistry , Insulin , Muscles , Penis , Protein Isoforms , Rats, Inbred OLETF , RNA, Messenger , Testosterone , Tissue DistributionABSTRACT
PURPOSE: To investigate the tissue distribution of PDE5 isoforms in type 2 diabetic rat penile tissues. MATERIALS AND METHODS: We prepared ten male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which develop NIDDM naturally, and ten control male Long-Evans Tokushima Fatty (LETO) rats. An oral glucose tolerance test confirmed diabetes development in OLETF rats at 26 weeks. At 42 weeks, we checked serum glucose, testosterone, triglyceride, insulin, and adiponectin before sacrifice. We performed semi-quantitative multiplex RT-PCR for rat PDE5, PDE5A1, and PDE5A2. Immunohistochemistry was performed using mouse monoclonal anti-cGB-PDE5 and anti-smooth muscle alpha-actin. RESULTS: OLETF rats were significantly more hyperglycemic, hypogonadal, hyperinsulinemic, hypercholesterolemic, hypertriglycemic, and had lower adiponectin levels than LETO rats. Levels of PDE5 mRNA were decreased in OLETF rats, but there were no changes in PDE5A1 or PDE5A2 mRNA levels. CONCLUSION: Diabetes may contribute to decreased expression of PDE5 mRNA, but not PDE5A1 or PDE5A2, in rat penile tissue. Furthermore, serum free testosterone was decreased in diabetic rats. PDE5 has an important role in the development of diabetic erectile dysfunction, but it is not clear whether PDE5A1 and PDE5A2 gene have specific roles.