Contemporary Evaluation and Management of Diabetic Cystopathy

Abstract

The M(3) receptor (M(3)-mAChR) is the major muscarinic subtype in the animal bladder responsible for detrusor contraction. The alterations in its protein quantity and biosynthesis during diabetic cystopathy were investigated. Three-month-old male Wistar rats were divided into two groups: (1) 2-week diabetic rats and (2) normoglycemic control rats. Diabetes was induced by a single intravenous injection of 60 mg/kg streptozotocin. The amount of M(3) receptor protein in the rat bladder body tissue was measured by Western immunoblotting using monoclonal antibodies. For determination of M(3) muscarinic receptor mRNA in the bladder tissue, the method of Northern blotting was employed. The results of the Western immunoblotting showed that the amount of M(3)-mAChR protein in the diabetic bladder was significantly increased by about 70.2 +/− 8.5 % when compared to the control bladder (p < 0.05, n = 8). Northern blotting demonstrated a 54.7 +/− 6.0 % increase of M(3)-mAChR mRNA in the diabetic bladder (p < 0.05, n = 8). The findings of the present study demonstrated an upregulation of M(3)-mAChR biosynthesis in the diabetic urinary bladder. This phenomenon offers an explanation of the increased contractility after muscarinic stimulation of the detrusor muscle of diabetic animals in human diabetic cystopathy as clasically described consists of triad of decreased bladder sensation, increased capacity and impaired detrusor contractility; however it is now clear that significant number of patients will have overactive bladder. High clinical suspicion and referal for urodynamics will allow improved diagnosis and treatment of bladder dysfunction.